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1
Roth, Joachim, Tunay Aslan, Birgit Störr та Eugen Zeisberger. "Lack of cross tolerance between LPS and muramyl dipeptide in induction of circulating TNF-α and IL-6 in guinea pigs". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, № 4 (1997): R1529—R1533. http://dx.doi.org/10.1152/ajpregu.1997.273.4.r1529.
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In guinea pigs, lipopolysaccharide (LPS) from gram-negative bacteria and muramyl dipeptide (MDP) from gram-positive bacteria are potent inducers of systemic production of proinflammatory cytokines and fever. However, there is a striking difference between these two bacterial pyrogens in so far as repeated administration of LPS, but not of MDP, in short-term intervals induces tolerance by a progressive downregulation of the systemic cytokine network. In the present study, we investigated MDP-induced fever and the systemic release of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in LPS-tolerant guinea pigs in comparison with naive animals. Endotoxin tolerance was induced by repeated intramuscular injections of 20 μg/kg LPS at intervals of 3 days. In response to the last of five injections with LPS, systemic production of TNF-α and IL-6 as well as the development of a febrile response was abrogated almost completely. Those guinea pigs that had developed an LPS tolerance could, however, produce the same amounts of TNF-α and IL-6 as naive animals in response to a challenge with MDP. Also, MDP-induced fever was identical in LPS-tolerant and naive guinea pigs. These results provide evidence for a lack of cross tolerance between LPS and MDP in induction of circulating cytokines and fever in guinea pigs.
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Sonoda, Koh-Hei, Mark Exley, Scott Snapper, Steven P. Balk, and Joan Stein-Streilein. "Cd1-Reactive Natural Killer T Cells Are Required for Development of Systemic Tolerance through an Immune-Privileged Site." Journal of Experimental Medicine 190, no. 9 (1999): 1215–26. http://dx.doi.org/10.1084/jem.190.9.1215.
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Systemic tolerance can be elicited by introducing antigen into an immune-privileged site, such as the eye, or directly into the blood. Both routes of immunization result in a selective deficiency of systemic delayed type hypersensitivity. Although the experimental animal model of anterior chamber–associated immune deviation (ACAID) occurs in most mouse strains, ACAID cannot be induced in several mutant mouse strains that are coincidentally deficient in natural killer T (NKT) cells. Therefore, this model for immune-privileged site–mediated tolerance provided us with an excellent format for studying the role of NKT cells in the development of tolerance. The following data show that CD1-reactive NKT cells are required for the development of systemic tolerance induced via the eye as follows: (a) CD1 knockout mice were unable to develop ACAID unless they were reconstituted with NKT cells together with CD1+ antigen-presenting cells; (b) specific antibody depletion of NKT cells in vivo abrogated the development of ACAID; and (c) anti-CD1 monoclonal antibody treatment of wild-type mice prevented ACAID development. Significantly, CD1-reactive NKT cells were not required for intravenously induced systemic tolerance, thereby establishing that different mechanisms mediate development of tolerance to antigens inoculated by these routes. A critical role for NKT cells in the development of systemic tolerance associated with an immune-privileged site suggests a mechanism involving NKT cells in self-tolerance and their defects in autoimmunity.
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Grdic, Dubravka, Elisabeth Hörnquist, Martin Kjerrulf, and Nils Y. Lycke. "Lack of Local Suppression in Orally Tolerant CD8-Deficient Mice Reveals a Critical Regulatory Role of CD8+ T Cells in the Normal Gut Mucosa." Journal of Immunology 160, no. 2 (1998): 754–62. http://dx.doi.org/10.4049/jimmunol.160.2.754.
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Abstract We found that feeding keyhole limpet hemocyanin (KLH) to CD8-deficient (CD8−/−) mice induced oral tolerance that was comparable in both magnitude and quality to that induced in wild-type (wt) mice. The tolerance was dose dependent, and only higher doses of KLH caused significant reduction in specific Ab and T cell responses. Both Th1 and Th2 CD4+ T cell functions were affected. Feeding KLH together with cholera toxin (CT) adjuvant, however, abrogated the induction of oral tolerance equally well in CD8−/− and wt mice. On the contrary, CT adjuvant was unable to abrogate already established oral tolerance in both CD8−/− and wt mice. Most importantly, whereas Ag feeding induced hyporesponsiveness in systemic as well as in local gut IgA responses in wt mice, a lack of local suppression was evident in orally tolerant CD8−/− mice following oral immunizations. Thus, contrary to the situation in wt mice, Ag feeding induces systemic, but not local, gut IgA hyporesponsiveness in CD8−/− mice, suggesting that CD8+ T cells in the normal gut mucosa exert an important down-regulatory function. In wt mice the local suppression extended to an unrelated Ag, OVA, given together with KLH and CT adjuvant, i.e., bystander suppression. Based on these results we propose that tolerance induced by feeding Ag is highly compartmentalized, requiring CD8+ T cells for local suppression of IgA responses, whereas systemic tolerance may affect CD4+ T cells of both Th1 and Th2 types independently of CD8+ T cells. Finally, the adjuvant effect of CT abrogates induction, but not established, oral tolerance through a mechanism that does not require CD8+ T cells.
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Zeng, Zhutian, Lu Li, Yongyan Chen, Haiming Wei, Rui Sun та Zhigang Tian. "Interferon-γ facilitates hepatic antiviral T cell retention for the maintenance of liver-induced systemic tolerance". Journal of Experimental Medicine 213, № 6 (2016): 1079–93. http://dx.doi.org/10.1084/jem.20151218.
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Persistent exposure to liver pathogens leads to systemic antigen-specific tolerance, a major cause of chronicity during hepatotropic infection. The mechanism regarding how this systemic tolerance is maintained remains poorly elucidated. In a well established mouse model of hepatitis B virus (HBV) persistence–induced systemic tolerance, we observed that interferon-γ (IFN-γ) deficiency led to complete loss of tolerance, resulting in robust anti-HBV responses upon peripheral vaccination. The recovery of vaccine-induced anti-HBV responses was mainly caused by the retained antigen-specific CD4+ T cells rather than decreased functional inhibitory cells in the periphery. Mechanistically, HBV persistence induced sustained hepatic CD4+ T cell–derived IFN-γ production. IFN-γ was found to promote CXCL9 secretion from liver-resident macrophages. This T cell chemokine facilitated the retention of antiviral CD4+ T cells in the liver in a CXCR3-dependent manner. Hepatic sequestrated antiviral CD4+ T cells subsequently underwent local apoptotic elimination partially via cytotoxic T lymphocyte–associated protein 4 ligation. These findings reveal an unexpected tolerogenic role for IFN-γ during viral persistence in the liver, providing new mechanistic insights regarding the maintenance of systemic antigen-specific tolerance during HBV persistence.
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Freise, Nicole, Alina Burghard, Theresa Ortkras, et al. "Signaling mechanisms inducing hyporesponsiveness of phagocytes during systemic inflammation." Blood 134, no. 2 (2019): 134–46. http://dx.doi.org/10.1182/blood.2019000320.
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Abstract The inflammatory responsiveness of phagocytes to exogenous and endogenous stimuli is tightly regulated. This regulation plays an important role in systemic inflammatory response syndromes (SIRSs). In SIRSs, phagocytes initially develop a hyperinflammatory response, followed by a secondary state of hyporesponsiveness, a so-called “tolerance.” This hyporesponsiveness can be induced by endotoxin stimulation of Toll-like receptor 4 (TLR4), resulting in an ameliorated response after subsequent restimulation. This modification of inflammatory response patterns has been described as innate immune memory. Interestingly, tolerance can also be triggered by endogenous TLR4 ligands, such as the alarmins myeloid-related protein 8 (MRP8, S100A8) and MRP14 (S100A9), under sterile conditions. However, signaling pathways that trigger hyporesponsiveness of phagocytes in clinically relevant diseases are only barely understood. Through our work, we have now identified 2 main signaling cascades that are activated during MRP-induced tolerance of phagocytes. We demonstrate that the phosphatidylinositol 3-kinase/AKT/GSK-3β pathway interferes with NF-κB–driven gene expression and that inhibition of GSK-3β mimics tolerance in vivo. Moreover, we identified interleukin-10–triggered activation of transcription factors STAT3 and BCL-3 as master regulators of MRP-induced tolerance. Accordingly, patients with dominant-negative STAT3 mutations show no tolerance development. In a clinically relevant condition of systemic sterile stress, cardiopulmonary bypass surgery, we confirmed the initial induction of MRP expression and the tolerance induction of monocytes associated with nuclear translocation of STAT3 and BCL-3 as relevant mechanisms. Our data indicate that the use of pharmacological JAK-STAT inhibitors may be promising targets for future therapeutic approaches to prevent complications associated with secondary hyporesponsiveness during SIRS.
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Shi, Hai Ning, Christian J. Ingui, Ingrid Dodge, and Cathryn Nagler-Anderson. "A Helminth-Induced Mucosal Th2 Response Alters Nonresponsiveness to Oral Administration of a Soluble Antigen." Journal of Immunology 160, no. 5 (1998): 2449–55. http://dx.doi.org/10.4049/jimmunol.160.5.2449.
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Abstract A fascinating feature of the intestinal mucosal immune system is its ability to guard against invasion by pathogens while avoiding a response to the many potential Ags present in food. The phenomenon of systemic tolerance after oral administration of protein Ags is well documented, but the cellular and molecular basis for the observed nonresponsiveness is not fully understood. To gain insight into the role of the mucosal microenvironment in the induction of orally induced nonresponsiveness, we attempted to induce tolerance to OVA in mice primed for a Th2-biased mucosal immune response by infection with the nematode parasite Heligmosomoides polygyrus. We found that oral tolerance for Th1-type responses to OVA is maintained when OVA is fed during the peak of the mucosal immune response to H. polygyrus. Tolerance for Th2 cytokine responses or a Th2-dependent isotype of IgG is not induced in this Th2-biased mucosal environment. Treatment of infected mice with rIL-12 to reverse the Th2 polarity of the parasite-specific immune response restores tolerance of both Th1 and Th2 responses to OVA. We conclude that the polarized Th2 response induced by this enteric infection plays a central role in determining whether or not systemic tolerance is induced. Our results imply that attempts to use oral administration of Ag to suppress systemic immune responses will be influenced strongly by the presence of mucosal infection.
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Cho, Song Mi, Beom Ryong Kang, Song Hee Han, et al. "2R,3R-Butanediol, a Bacterial Volatile Produced by Pseudomonas chlororaphis O6, Is Involved in Induction of Systemic Tolerance to Drought in Arabidopsis thaliana." Molecular Plant-Microbe Interactions® 21, no. 8 (2008): 1067–75. http://dx.doi.org/10.1094/mpmi-21-8-1067.
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Root colonization of plants with certain rhizobacteria, such as Pseudomonas chlororaphis O6, induces tolerance to biotic and abiotic stresses. Tolerance to drought was correlated with reduced water loss in P. chlororaphis O6-colonized plants and with stomatal closure, indicated by size of stomatal aperture and percentage of closed stomata. Stomatal closure and drought resistance were mediated by production of 2R,3R-butanediol, a volatile metabolite of P. chlororaphis O6. Root colonization with bacteria deficient in 2R,3R-butanediol production showed no induction of drought tolerance. Studies with Arabidopsis mutant lines indicated that induced drought tolerance required the salicylic acid (SA)-, ethylene-, and jasmonic acid-signaling pathways. Both induced drought tolerance and stomatal closure were dependent on Aba-1 and OST-1 kinase. Increases in free SA after drought stress of P. chlororaphis O6-colonized plants and after 2R,3R-butanediol treatment suggested a primary role for SA signaling in induced drought tolerance. We conclude that the bacterial volatile 2R,3R-butanediol was a major determinant in inducing resistance to drought in Arabidopsis through an SA-dependent mechanism.
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Issazadeh, Shohreh, ManHua Zhang, Mohamed H. Sayegh, and Samia J. Khoury. "Acquired Thymic Tolerance: Role of CTLA4 in the Initiation and Maintenance of Tolerance in a Clinically Relevant Autoimmune Disease Model." Journal of Immunology 162, no. 2 (1999): 761–65. http://dx.doi.org/10.4049/jimmunol.162.2.761.
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Abstract Injection of Ag into the thymus of adult animals induces specific systemic tolerance. The mechanisms of acquired thymic tolerance include anergy and the deletion of Ag-specific T cells. Here, we report that anergy to nominal Ag induced via acquired thymic tolerance requires CTL-associated Ag 4 (CTLA4) engagement. The role of CTLA4 in the induction and maintenance of tolerance was then investigated in the murine experimental autoimmune encephalomyelitis model. CTLA4 blockade abrogated the induction but not the maintenance phase of acquired thymic tolerance induced by intrathymic injection of myelin Ags. In addition, CTLA4 blockade had a restricted window of action after priming with Ag, which is consistent with the expression patterns of CTLA4 in vivo. We conclude that: 1) the induction of acquired thymic tolerance requires signaling through CTLA4 and 2) CTLA4 does not appear to be required for the maintenance of acquired thymic tolerance. This is the first report documenting the role of a CTLA4 negative signaling pathway in the induction of tolerance in an autoimmune disease model.
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Husby, S., J. Mestecky, Z. Moldoveanu, S. Holland, and C. O. Elson. "Oral tolerance in humans. T cell but not B cell tolerance after antigen feeding." Journal of Immunology 152, no. 9 (1994): 4663–70. http://dx.doi.org/10.4049/jimmunol.152.9.4663.
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Abstract The purpose of this study was to investigate whether oral tolerance, defined as Ag-specific immunologic unresponsiveness after Ag feeding, could be induced in humans after prolonged Ag ingestion. Eight adult volunteers ingested a total dose of 0.5 g of keyhole limpet hemocyanin (KLH) followed by subcutaneous immunization with KLH. Eight controls received only the subcutaneous immunization. In the group fed KLH, there was a significant reduction in KLH-specific T cell proliferation (p = 0.04) and delayed skin test responses (p = 0.07) to KLH. KLH ingestion alone did not induce significant levels of Abs in either serum or secretions. However, after the subsequent subcutaneous immunization, the number of circulating IgG and IgM anti-KLH-producing cells, the titers of serum IgG, IgA, and IgM anti-KLH Abs, and the titers of IgA anti-KLH Abs in saliva and intestinal secretions were significantly greater in the KLH-fed group than in the nonfed group. We conclude that KLH feeding induced systemic T cell tolerance, but B cell priming, at both systemic and mucosal sites. These studies support the concept of using Ag feeding as a treatment for certain immune-mediated diseases.
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Zhang, Jun, Yunxia Wang, and Xin Qi. "Systemic Rapamycin Attenuates Morphine-Induced Analgesic Tolerance and Hyperalgesia in Mice." Neurochemical Research 44, no. 2 (2018): 465–71. http://dx.doi.org/10.1007/s11064-018-2699-0.
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Lilius, Tuomas O., Pekka V. Rauhala, Oleg Kambur, and Eija A. Kalso. "Modulation of Morphine-induced Antinociception in Acute and Chronic Opioid Treatment by Ibudilast." Anesthesiology 111, no. 6 (2009): 1356–64. http://dx.doi.org/10.1097/aln.0b013e3181bdfa11.
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Background Opioid analgesics are effective in relieving chronic pain, but they have serious adverse effects, including development of tolerance and dependence. Ibudilast, an inhibitor of glial activation and cyclic nucleotide phosphodiesterases, has shown potential in the treatment of neuropathic pain and opioid withdrawal. Because glial cell activation could also be involved in the development of opioid tolerance in rats, the authors studied the antinociceptive effects of ibudilast and morphine in different models of coadministration. Methods Antinociception was assessed using male Sprague- Dawley rats in hot plate and tail-flick tests. The effects of ibudilast on acute morphine-induced antinociception, induction of morphine tolerance, and established morphine tolerance were studied. Results Systemic ibudilast produced modest dose-related antinociception and decreased locomotor activity at the studied doses of 2.5-22.5 mg/kg. The highest tested dose of 22.5 mg/kg produced 52% of the maximum possible effect in the tail-flick test. It had an additive antinociceptive effect when combined with systemic morphine. Coadministration of ibudilast with morphine did not attenuate the development of morphine tolerance. However, in morphine-tolerant rats, ibudilast partly restored morphine-induced antinociception. Conclusions Ibudilast produces modest antinociception, and it is effective in restoring but not in preventing morphine tolerance. The mechanisms of the effects of ibudilast should be better understood before it is considered for clinical use.
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Vazquez-Rodriguez, E., K. Ramirez, C. Avila, W. Escobar, H. Vanegas, and V. Tortorici. "322 REPEATED MORPHINE ADMINISTRATION INDUCED ANALGESIC TOLERANCE TO MORPHINE AND CROSS TOLERANCE TO SYSTEMIC DIPYRONE (METAMIZOL)." European Journal of Pain 10, S1 (2006): S86a—S86. http://dx.doi.org/10.1016/s1090-3801(06)60325-x.
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Marth, T., W. Strober, and B. L. Kelsall. "High dose oral tolerance in ovalbumin TCR-transgenic mice: systemic neutralization of IL-12 augments TGF-beta secretion and T cell apoptosis." Journal of Immunology 157, no. 6 (1996): 2348–57. http://dx.doi.org/10.4049/jimmunol.157.6.2348.
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Abstract The immune response to oral Ag administration, including the development of oral tolerance, was explored with the use of OVA TCR-transgenic mice. Feeding high doses of OVA enhanced IFN-gamma production in the Peyer's patches, but induced tolerance in the peripheral lymphoid tissues marked by suppressed proliferative and cytokine responses. Systemic administration of Abs to IL-12 (anti-IL-12) simultaneous with Ag feeding modestly enhanced the degree of tolerance in the peripheral lymphoid tissues, as shown by increased suppression of proliferative responses after in vitro restimulation, and secondary responses in the popliteal lymph nodes following in vivo challenge and in vitro restimulation. Systemic anti-IL-12 treatment was associated with augmented TGF-beta production and T cell apoptosis in both Peyer's patches and peripheral lymphoid tissues. Cell mixing studies and proliferation assays in the presence of anti-TGF-beta provided evidence that the increased suppression of responses induced by anti-IL-12 was due primarily to the secretion of TGF-beta. These findings suggest that IL-12 negatively regulates two of the main mechanisms of oral tolerance, TGF-beta production and clonal deletion via apoptosis. in addition, they suggest that the combination of oral Ag feeding and systemic anti-IL-12 administration may be of benefit in the treatment of autoimmune diseases.
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Liang, De-Yong, XiangQi Li, and J. David Clark. "5-Hydroxytryptamine Type 3 Receptor Modulates Opioid-induced Hyperalgesia and Tolerance in Mice." Anesthesiology 114, no. 5 (2011): 1180–89. http://dx.doi.org/10.1097/aln.0b013e31820efb19.
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Background Opioid-induced hyperalgesia (OIH) and tolerance are challenging maladaptations associated with opioids in managing pain. Recent genetic studies and the existing literature suggest the 5-hydroxytryptamine type 3 (5-HT3) receptor participates in these phenomena. The location of the relevant receptor populations and the interactions between the 5-HT3 system and other systems controlling OIH and tolerance have not been explored, however. We hypothesized that 5-HT3 receptors modulate OIH and tolerance, and that this modulation involves the control of expression of multiple neurotransmitter and receptor systems. Methods C57BL/6 mice were exposed to a standardized 4-day morphine administration protocol. The 5-HT3 antagonist ondansetron was administered either during or after the conclusion of morphine administration. Mechanical testing was used to quantify OIH, and thermal tail-flick responses were used to measure morphine tolerance. In other experiments spinal cord and dorsal root ganglion tissues were harvested for analysis of messenger RNA concentrations by real-time polymerase chain reaction or immunochemistry analysis. Results The results showed that (1) systemic or intrathecal injection of ondansetron significantly prevented and reversed OIH, but not local intraplantar injection; (2) systemic or intrathecal injection of ondansetron prevented and reversed tolerance; and (3) ondansetron blocked morphine-induced increases of multiple genes relevant to OIH and tolerance in dorsal root ganglion and spinal cord. Conclusions Morphine acts via a 5-HT3-dependent mechanism to support multiple maladaptations to the chronic administration of morphine. Furthermore, the use of 5-HT3 receptor antagonists may provide a new avenue to prevent or reverse OIH and tolerance associated with chronic opioid use.
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Mowat, Allan McI, Margaret Steel, Andrew J. Leishman та Paul Garside. "Normal Induction of Oral Tolerance in the Absence of a Functional IL-12-Dependent IFN-γ Signaling Pathway". Journal of Immunology 163, № 9 (1999): 4728–36. http://dx.doi.org/10.4049/jimmunol.163.9.4728.
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Abstract There is considerable evidence that regulatory cytokines play an important role in mediating the systemic tolerance found after oral administration of protein Ags. Although most existing work has focused on cytokines such as IL-4, IL-10, and TGF-β, recent evidence from TCR transgenic systems suggests that the induction of oral tolerance is accompanied by priming of Ag-specific IFN-γ production. IFN-γ has also been implicated as a mediator of T cell tolerance in other models in vivo and in vitro, including that induced by aerosol administration of protein. We show here that feeding tolerogenic doses of OVA primes for IFN-γ production in the spleen of mice with a normal T cell repertoire. However, depleting IFN-γ at the time of feeding OVA had no effect on the induction of tolerance. In addition, tolerance was induced normally in both IFN-γ receptor knockout (IFN-γR−/−) and IL-12 p40 knockout (IL-12−/−) mice. This was the case for all components of the systemic immune response and also with a variety of feeding protocols, including those believed to induce distinct regulatory mechanisms. We conclude that IL-12-dependent IFN-γ-mediated regulation does not play an essential role in oral tolerance.
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Feuerstein, Nili, Fangqi Chen, Michael Madaio, Michael Maldonado, and Robert A. Eisenberg. "Induction of Autoimmunity in a Transgenic Model of B Cell Receptor Peripheral Tolerance: Changes in Coreceptors and B Cell Receptor-Induced Tyrosine-Phosphoproteins." Journal of Immunology 163, no. 10 (1999): 5287–97. http://dx.doi.org/10.4049/jimmunol.163.10.5287.
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Abstract Abrogation of peripheral tolerance in transgenic mice that express a uniform B-cell receptor may create a powerful tool to examine the molecular mechanisms that underlie the autoimmune response in B cells. Here we report that processes that induce a systemic lupus erythematosus-like syndrome in normal mice, namely chronic graft vs host reaction, trigger systemic autoimmunity in a well-established transgenic mice model of B cell receptor peripheral tolerance. The induction of graft vs host reaction in mice that carry both a rearranged B cell Ag receptors specific for hen egg lysozyme and expressing chronically circulating hen egg lysozyme Ag resulted in induction of high and sustained levels of circulating anti-hen egg lysoyme autoantibodies and glomerulonephritis with proteinuria. This was associated with marked changes in expression of cell-surface proteins, such as CD23 and complement receptor 2. B cells from the graft vs host-induced mice could proliferate in vitro in response to self-Ag, and upon stimulation with anti-IgD demonstrated rapid phosphotyrosine phosphorylation of specific proteins, which could not be induced in the anergic double transgenic B cells. Conversely, loss of tolerance was not associated with a higher induction in the level of Syk kinase phosphorylation following stimulation with anti-IgD. Taken collectively, these data establish that 1) processes that induce a systemic lupus erythematosus-like syndrome in normal mice can abrogate peripheral tolerance in transgenic mice expressing self-tolerized B cells, and that 2) loss of tolerance in this model is associated with marked changes in surface expression of B cell coreceptors as well as with selective changes in IgD-induced signaling by discrete tyrosine-phosphoproteins, but not Syk kinase.
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Li, Shalan, Jingxiong Zhang, Hui Liu, et al. "Dodder-transmitted mobile signals prime host plants for enhanced salt tolerance." Journal of Experimental Botany 71, no. 3 (2019): 1171–84. http://dx.doi.org/10.1093/jxb/erz481.
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Abstract The dodders (Cuscuta spp.) are a genus of shoot parasites. In nature, a dodder often simultaneously parasitizes two or more neighboring hosts. Salt stress is a common abiotic stress for plants. It is unclear whether dodder transmits physiologically relevant salt stress-induced systemic signals among its hosts and whether these systemic signals affect the hosts’ tolerance to salt stress. Here, we simultaneously parasitized two or more cucumber plants with dodder. We found that salt treatment of one host highly primed the connected host, which showed strong decreases in the extent of leaf withering and cell death in response to subsequent salt stress. Transcriptomic analysis indicated that 24 h after salt treatment of one cucumber, the transcriptome of the other dodder-connected cucumber largely resembled that of the salt-treated one, indicating that inter-plant systemic signals primed these dodder-connected cucumbers at least partly through transcriptomic reconfiguration. Furthermore, salt treatment of one of the cucumbers induced physiological changes, including altered proline contents, stomatal conductance, and photosynthetic rates, in both of the dodder-connected cucumbers. This study reveals a role of dodder in mediating salt-induced inter-plant signaling among dodder-connected hosts and highlights the physiological function of these mobile signals in plant–plant interactions under salt stress.
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Yu, Jin, Hong Zhu, Saeid Taheri, William Mondy, Stephen Perry, and Mark S. Kindy. "Plant-Based Nutritional Supplementation Attenuates LPS-Induced Low-Grade Systemic Activation." International Journal of Molecular Sciences 22, no. 2 (2021): 573. http://dx.doi.org/10.3390/ijms22020573.
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Plant-based nutritional supplementation has been shown to attenuate and reduce mortality in the processes of both acute and chronic disorders, including diabetes, obesity, cardiovascular disease, cancer, inflammatory diseases, and neurological and neurodegenerative disorders. Low-level systemic inflammation is an important contributor to these afflictions and diets enriched in phytochemicals can slow the progression. The goal of this study was to determine the impact of lipopolysaccharide (LPS)-induced inflammation on changes in glucose and insulin tolerance, performance enhancement, levels of urinary neopterin and concentrations of neurotransmitters in the striatum in mouse models. Both acute and chronic injections of LPS (2 mg/kg or 0.33 mg/kg/day, respectively) reduced glucose and insulin tolerance and elevated neopterin levels, which are indicative of systemic inflammatory responses. In addition, there were significant decreases in striatal neurotransmitter levels (dopamine and DOPAC), while serotonin (5-HT) levels were essentially unchanged. LPS resulted in impaired execution in the incremental loading test, which was reversed in mice on a supplemental plant-based diet, improving their immune function and maintaining skeletal muscle mitochondrial activity. In conclusion, plant-based nutritional supplementation attenuated the metabolic changes elicited by LPS injections, causing systemic inflammatory activity that contributed to both systemic and neurological alterations.
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Yu, Jin, Hong Zhu, Saeid Taheri, William Mondy, Stephen Perry, and Mark S. Kindy. "Plant-Based Nutritional Supplementation Attenuates LPS-Induced Low-Grade Systemic Activation." International Journal of Molecular Sciences 22, no. 2 (2021): 573. http://dx.doi.org/10.3390/ijms22020573.
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Plant-based nutritional supplementation has been shown to attenuate and reduce mortality in the processes of both acute and chronic disorders, including diabetes, obesity, cardiovascular disease, cancer, inflammatory diseases, and neurological and neurodegenerative disorders. Low-level systemic inflammation is an important contributor to these afflictions and diets enriched in phytochemicals can slow the progression. The goal of this study was to determine the impact of lipopolysaccharide (LPS)-induced inflammation on changes in glucose and insulin tolerance, performance enhancement, levels of urinary neopterin and concentrations of neurotransmitters in the striatum in mouse models. Both acute and chronic injections of LPS (2 mg/kg or 0.33 mg/kg/day, respectively) reduced glucose and insulin tolerance and elevated neopterin levels, which are indicative of systemic inflammatory responses. In addition, there were significant decreases in striatal neurotransmitter levels (dopamine and DOPAC), while serotonin (5-HT) levels were essentially unchanged. LPS resulted in impaired execution in the incremental loading test, which was reversed in mice on a supplemental plant-based diet, improving their immune function and maintaining skeletal muscle mitochondrial activity. In conclusion, plant-based nutritional supplementation attenuated the metabolic changes elicited by LPS injections, causing systemic inflammatory activity that contributed to both systemic and neurological alterations.
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Sharon, Andrew J., Heather A. Filyk, Nicolette M. Fonseca, et al. "STAT1-dependent tolerance of intestinal viral infection." Journal of Immunology 204, no. 1_Supplement (2020): 249.11. http://dx.doi.org/10.4049/jimmunol.204.supp.249.11.
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Abstract The diverse commensal ecosystem present in the mammalian intestine requires the host immune system to maintain a tolerogenic environment. The virome is an understudied component of the microbiota which promotes intestinal homeostasis and protection from injury, but the host mechanisms that regulate tolerance to viral commensals are poorly described. The antiviral signal transducer STAT1 has previously been shown to mediate tolerance to systemic viral pathogens by suppressing adaptive immune responses and protecting the host from immunopathology, but we sought to characterize its role in the context of a commensal intestinal viral infection. We used a persistent strain of murine norovirus (MNV CR6) to interrogate host mechanisms of viral tolerance and commensalism, as CR6 has previously been shown to promote intestinal homeostasis. While CR6 infections of wildtype mice were asymptomatic and limited to the colon, STAT1-deficient mice exhibited virus-induced weight loss and mortality accompanied by systemic viral spread, colonic bacterial dysbiosis, CD4+ T cell dysfunction and hyperaccumulation of CD8+ T cells. However, clinical manifestation of virus-induced disease in STAT1-deficient mice was independent of T cells and the bacterial microbiota. Instead, therapeutic control of viral replication was sufficient to prevent virus-induced disease despite ongoing T cell dysregulation. Collectively, our data indicate that STAT1 maintains tolerance to a viral component of the intestinal microbiota by control of viral replication rather than immunopathology, suggesting that STAT1 uses distinct strategies to tolerate pathogenic and commensal viruses.
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Cheng, Yuan, Xin Li, Ming-Ya Fang, Qing-Jing Ye, Zhi-Miao Li, and Golam Jalal Ahammed. "Systemic H2O2 signaling mediates epigallocatechin-3-gallate-induced cadmium tolerance in tomato." Journal of Hazardous Materials 438 (September 2022): 129511. http://dx.doi.org/10.1016/j.jhazmat.2022.129511.
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Carlson, René, Fidele Tugizimana, Paul A. Steenkamp, Ian A. Dubery, Ahmed Idris Hassen, and Nico Labuschagne. "Rhizobacteria-induced systemic tolerance against drought stress in Sorghum bicolor (L.) Moench." Microbiological Research 232 (February 2020): 126388. http://dx.doi.org/10.1016/j.micres.2019.126388.
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Zhang, Huang-ge, Xiao Su, Di Liu, et al. "Induction of Specific T Cell Tolerance by Fas Ligand- Expressing Antigen-Presenting Cells." Journal of Immunology 162, no. 3 (1999): 1423–30. http://dx.doi.org/10.4049/jimmunol.162.3.1423.
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Abstract Autocrine interaction of Fas and Fas ligand leads to apoptosis of activated T cells, a process that is critical for the maintenance of peripheral T cell tolerance. Paracrine interactions of Fas ligand with T cells also may play an important role in the maintenance of tolerance, as Fas ligand can create immune-privileged sites and prevent graft rejection by inducing apoptosis in T cells. We surmised that APCs that express Fas ligand might directly induce apoptosis of T cells during presentation of Ag to the T cells, thus inducing Ag-specific, systemic T cell tolerance. Here, we show that profound, specific T cell unresponsiveness to alloantigen was induced by treatment of H-2k mice with H-2b APCs that expressed Fas ligand and that profound T cell unresponsiveness specific for the H-Y Ag was induced by treatment of H-2Db/H-Y TCR transgenic female mice with H-2Db/H-Y APCs that expressed Fas ligand. The induction of this systemic T cell tolerance required the expression of Fas ligand on the APCs as well as the expression of Fas on the T cells. The tolerance was restricted to the Ag presented by the APCs. The rapid and profound clonal deletion of the Ag-specific, peripheral T cells mediated by the Fas ligand-expressing APCs contributed to the induction of tolerance. These findings demonstrate that Ag-specific T cell tolerance can be induced by APCs that express Fas ligand and suggest a novel function for APCs in the induction of T cell apoptosis. Furthermore, they indicate a novel immunointervention strategy for treatment of graft rejection and autoantigen-specific autoimmune diseases.
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Kawano, Takayuki, Alexander Kunz, Takato Abe, et al. "iNOS-Derived NO and Nox2-Derived Superoxide Confer Tolerance to Excitotoxic Brain Injury through Peroxynitrite." Journal of Cerebral Blood Flow & Metabolism 27, no. 8 (2007): 1453–62. http://dx.doi.org/10.1038/sj.jcbfm.9600449.
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Sublethal injurious stimuli induce tolerance to subsequent lethal insults, a phenomenon termed preconditioning. Inducible nitric oxide synthase (iNOS) is essential for the preconditioning induced by transient bilateral common carotid artery occlusion (BCCAO) or by systemic administration of the endotoxin lipopolysaccharide (LPS). We used a model of brain injury produced by neocortical injection of N-methyl-d-aspartate (NMDA) to investigate the mechanisms by which iNOS-derived nitric oxide (NO) contributes to tolerance induced by LPS or BCCAO. We found that the tolerance is blocked by the iNOS inhibitor aminoguanidine, is not observed in iNOS-null mice, and is rescued by the NO donor DTPA NONOate. Lipopolysaccharide failed to induce preconditioning in mice lacking the nox2 subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, suggesting that superoxide derived from NADPH oxidase is needed for the induction of the tolerance. Because superoxide reacts with NO to form peroxynitrite, we investigated the role of peroxynitrite. We found that LPS induces the peroxynitrite marker 3-nitrotyrosine in cortical neurons and that the peroxynitrite decomposition catalyst FeTPPS abolishes LPS-induced preconditioning. These results suggest that the protective effect of iNOS-derived NO is mediated by peroxynitrite formed by the reaction of NO with NADPH oxidase-derived superoxide. Thus, peroxynitrite, in addition to its well-established deleterious role in ischemic brain injury and neurodegeneration, can also be beneficial by inducing tolerance to excitotoxicity.
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Thim-Uam, Arthid, Jiradej Makjaroen, Jiraphorn Issara-Amphorn, et al. "Enhanced Bacteremia in Dextran Sulfate-Induced Colitis in Splenectomy Mice Correlates with Gut Dysbiosis and LPS Tolerance." International Journal of Molecular Sciences 23, no. 3 (2022): 1676. http://dx.doi.org/10.3390/ijms23031676.
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Because both endotoxemia and gut dysbiosis post-splenectomy might be associated with systemic infection, the susceptibility against infection was tested by dextran sulfate solution (DSS)-induced colitis and lipopolysaccharide (LPS) injection models in splenectomy mice with macrophage experiments. Here, splenectomy induced a gut barrier defect (FITC-dextran assay, endotoxemia, bacteria in mesenteric lymph nodes, and the loss of enterocyte tight junction) and gut dysbiosis (increased Proteobacteria by fecal microbiome analysis) without systemic inflammation (serum IL-6). In parallel, DSS induced more severe mucositis in splenectomy mice than sham-DSS mice, as indicated by mortality, stool consistency, gut barrier defect, serum cytokines, and blood bacterial burdens. The presence of green fluorescent-producing (GFP) E. coli in the spleen of sham-DSS mice after an oral gavage supported a crucial role of the spleen in the control of bacteria from gut translocation. Additionally, LPS administration in splenectomy mice induced lower serum cytokines (TNF-α and IL-6) than LPS-administered sham mice, perhaps due to LPS tolerance from pre-existing post-splenectomy endotoxemia. In macrophages, LPS tolerance (sequential LPS stimulation) demonstrated lower cell activities than the single LPS stimulation, as indicated by the reduction in supernatant cytokines, pro-inflammatory genes (iNOS and IL-1β), cell energy status (extracellular flux analysis), and enzymes of the glycolysis pathway (proteomic analysis). In conclusion, a gut barrier defect after splenectomy was vulnerable to enterocyte injury (such as DSS), which caused severe bacteremia due to defects in microbial control (asplenia) and endotoxemia-induced LPS tolerance. Hence, gut dysbiosis and gut bacterial translocation in patients with a splenectomy might be associated with systemic infection, and gut-barrier monitoring or intestinal tight-junction strengthening may be useful.
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Ravishankar, Buvana, Haiyun Liu, Rahul Shinde, Phillip Chandler, and Tracy McGaha. "Innate and adaptive tolerance to apoptotic cells is controlled by an IDO- dependent mechanism. (123.49)." Journal of Immunology 188, no. 1_Supplement (2012): 123.49. http://dx.doi.org/10.4049/jimmunol.188.supp.123.49.
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Abstract Marginal zone macrophages (MZMs) play a crucial role in generation of systemic tolerance to apoptotic cell (AC)-associated antigens. However, the mechanism(s) by which MZMs drive tolerogenic responses is not understood. In this report, we show that systemic administration of ACs induces splenic expression of the immunosuppressive enzyme indoleamine 2-3 dioxygenase (IDO) in Marco+SignR1+ MZMs. Moreover, we found abrogation of IDO activity altered immunity to ACs resulting in decreased TGF-β synthesis and increased pro-inflammatory cytokine production associated with a reduction in Treg function and a loss of T cell tolerance towards AC antigens. When pre-symptomatic, lupus-prone MRLlpr/lpr mice were examined we found significant IDO expression in the splenic MZ analogous to the observations in AC challenged mice. When IDO was inhibited, autoimmunity was rapidly accelerated in MRLlpr/lpr mice with a >10-fold increase in anti-dsDNA IgG titers and increased renal pathology. Finally, IDO-/- mice, which do not show signs of autoimmunity, were challenged chronically with ACs. The mice developed high titer serum IgG autoreactivity, kidney inflammation, and increased mortality compared to B6 mice, which did not develop autoimmunity. Thus, the data demonstrate that a novel IDO-dependent regulatory circuit is induced in MZMs upon apoptotic cell phagocytosis providing clues to future therapeutic targets to re-establish tolerance in systemic autoimmune disease.
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Oelert, Thilo, Maria Papatriantafyllou, Georg Pougialis, Günter J. Hämmerling, Bernd Arnold, and Thomas Schüler. "Irradiation and IL-15 promote loss of CD8 T-cell tolerance in response to lymphopenia." Blood 115, no. 11 (2010): 2196–202. http://dx.doi.org/10.1182/blood-2009-06-227298.
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Abstract Functional inactivation of self-reactive T lymphocytes contributes to the maintenance of immunologic self-tolerance. At the same time, tolerance induction limits immune responses against tumors expressing tolerizing self-antigens. Some cancer therapies include the adoptive transfer of tumor-reactive T lymphocytes into lymphopenic patients. Lymphopenia provides an activation signal to T lymphocytes, which undergo lymphopenia-induced proliferation (LIP), acquire effector functions, and reject tumors. However, it is so far unknown to which extent LIP may result in reversal of established antigen-specific CD8 T-cell tolerance. Here, we report that neonatally induced dominant CD8 T-cell tolerance remained stable under lymphopenic conditions also in the presence of systemic inflammation induced by Toll-like receptor ligands. However, when lymphopenic recipients were irradiated, the tolerant status was lost, because CD8 T cells acquired effector functions in an interleukin-15–dependent fashion and efficiently rejected tumors. In conclusion, we show that lymphopenia is not sufficient to break CD8 T-cell tolerance. Furthermore, we demonstrate that pretreatment regimens are crucial to circumvent this problem and to optimize adoptive T-cell therapy.
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Aichele, P., K. Brduscha-Riem, R. M. Zinkernagel, H. Hengartner, and H. Pircher. "T cell priming versus T cell tolerance induced by synthetic peptides." Journal of Experimental Medicine 182, no. 1 (1995): 261–66. http://dx.doi.org/10.1084/jem.182.1.261.
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It is well known that synthetic peptides are able to both induce and tolerize T cells. We have examined the parameters leading either to priming or tolerance of CD8+ cytotoxic T lymphocytes (CTL) in vivo with a major histocompatibility complex class I (H-2 Db) binding peptide derived from the glycoprotein (GP aa33-41) of lymphocytic choriomeningitis virus (LCMV). By varying dose, route, and frequency of LCMV GP peptide application, we found that a single local subcutaneous injection of 50-500 micrograms peptide emulsified in incomplete Freund's adjuvant protected mice against LCMV infection, whereas repetitive and systemic intraperitoneal application of the same dose caused tolerance of LCMV-specific CTL. The peptide-induced tolerance was transient in euthymic mice but permanent in thymectomized mice. These findings are relevant for a selective use of peptides as a therapeutic approach: peptide-induced priming of T cells for vaccination and peptide-mediated T cell tolerance for intervention in immunopathologies and autoimmune diseases.
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Yoo, Sung-Je, and Mee Kyung Sang. "Induced Systemic Tolerance to Multiple Stresses Including Biotic and Abiotic Factors by Rhizobacteria." Research in Plant Disease 23, no. 2 (2017): 99–113. http://dx.doi.org/10.5423/rpd.2017.23.2.99.
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Krzikalla, Daria, Alena Laschtowitz, Lisa Leypoldt, et al. "Interferon-gamma and CTLA-4 drive liver-induced systemic CD4 T cell tolerance." Journal of Hepatology 73 (August 2020): S82. http://dx.doi.org/10.1016/s0168-8278(20)30694-2.
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Remuzzi, G., M. Noris, A. Benigni, O. Imberti, M. H. Sayegh, and N. Perico. "Thromboxane A2 receptor blocking abrogates donor-specific unresponsiveness to renal allografts induced by thymic recognition of major histocompatibility allopeptides." Journal of Experimental Medicine 180, no. 5 (1994): 1967–72. http://dx.doi.org/10.1084/jem.180.5.1967.
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Recent in vitro studies have documented that thromboxane (Tx)A2 induces thymocyte apoptosis by acting on specific receptors abundantly expressed on the surface of immature T lymphocytes. No information is available on the in vivo relevance of this observation in development of self- or acquired tolerance. We and others have previously documented that injection of donor cells into adult thymus of experimental animals induced specific systemic unresponsiveness to allografts in the rat and mouse models. More recently, we have shown that intrathymic injection of synthetic class II major histocompatibility complex (MHC) allopeptides resulted in donor-specific unresponsiveness to renal allografts. The induction of unresponsiveness was abrogated by recipient thymectomy within the first week. We now report the effect of TxA2 blockade on acquired thymic tolerance to renal allografts induced by intrathymic injection of synthetic class II MHC allopeptides in the Wistar-Furth (WF) to Lewis rat strain combination. Administration of the TxA2 receptor blocker prior to transplantation or 2 wk postengraftment completely abrogated the unresponsive state. In addition, inhibiting the TxA2-forming enzyme by aspirin or dexamethasone also abolished the induction of acquired thymic tolerance. Evidence is also provided for a critical "dose" of peptides to be injected into the thymus to induce systemic unresponsiveness to renal allografts. These data, coupled with observations that activated peripheral T cells can circulate through the thymus, provide evidence that TxA2/TxA2 receptor interaction in the thymic microenvironment, leading to anergy/programmed cell death of activated T cells, may play an important role in the development of acquired unresponsiveness in vivo.
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Gordon, John, Chunyan Li, Laura Churchman, and Wojciech Dawicki. "Reversal of peanut anaphylaxis by retinoic acid-differentiated dendritic cell immunotherapy. IL-27-dependent induction of Foxp3- non-Tr1 regulatory T cells (VAC4P.1100)." Journal of Immunology 194, no. 1_Supplement (2015): 72.5. http://dx.doi.org/10.4049/jimmunol.194.supp.72.5.
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Abstract Background. Semi-mature IL-10-induced DC (DC10) induce human or mouse effector Th2 cells (Teff) to differentiate into Foxp3+ Treg and thereby induce asthma tolerance. Retinoic acid (RA) and TGFβ-induced gut DC similarly induce tolerance to gut contents via Foxp3+ Treg, while immature hDC-10 induce IL-10-dependent Foxp3- Tr1 cells. Methods. We assessed the abilities of mature RA-induced DC to reverse anaphylaxis sensitivity, characterizing LPS-matured DC-RA and their tolerogenic activities in mouse models of OVA and peanut systemic anaphylaxis. Results. Mature DC-RA strongly expressed CD103 (αE integrin), MHCII, co-stimulatory markers, PDL1 & -L2, ICOSL, TGFβ, IL-27 and the RA-metabolizing enzyme Aldh1A2. They induced Th2 cells to convert into CD25+LAG3+CD49b-IL-10-Foxp3- Treg in an IL-10-independent, IL-27-dependent fashion, although IL-27 was dispensable for Th2 suppression by DC-RA. Wild-type, but not IL-27-/- DC-RA therapy reversed systemic anaphylaxis, including clinical scores, diarrhea, mast cell activation and Th2 responses, and lowered serum allergen-specific IgE and IgG1 levels. Conclusions. Allergen-presenting DC-RA induce food allergen tolerance by activating CD25+Foxp3-, non-Tr1 responses in an IL-27-dependent fashion. This data indicates that, like DC10, DC-RA can also be used for allergic disease immunotherapy, but that these two populations of DCreg induce distinct Treg responses, and this potentially provides us with important options DCreg immunotherapy
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Yamasaki, Satoshi, Yoshiaki Miura, Julia Davydova, Selwyn M. Vickers, and Masato Yamamoto. "A Single Intraduodenal Administration of Human Adenovirus 40 Vaccine Effectively Prevents Anaphylactic Shock." Clinical and Vaccine Immunology 20, no. 10 (2013): 1508–16. http://dx.doi.org/10.1128/cvi.00417-13.
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ABSTRACTVaccine administration into the intestine is known to induce mucosal tolerance most efficiently. Therefore, developing a delivery system that targets the intestinal mucosa is expected to improve the efficiency of immunosuppression. Human enteric adenovirus serotype 40 (Ad40)-based vectors have the advantage of targeting intestinal mucosa, making them prime candidates as mucosal vaccine carriers for immunosuppression. Here, after both oral and intraduodenal administrations, the vector distribution of replication-defective recombinant Ad40 vectors (rAd40) was significantly higher than that of a conventional Ad vector based on human adenovirus 5 (Ad5) in ilea containing Peyer's patches. Single intraduodenal administration of rAd40 induced antigen-specific mucosal immunoreaction mediated by intestinal mucosal and systemic immunity. In ovalbumin-induced allergy mouse models, this approach inhibited antigen-specific delayed-type hypersensitivity reactions, diarrhea occurrence, and systemic anaphylaxis. Thus, a single intraduodenal administration of rAd40 provides a potent method of inducing allergen-specific mucosal tolerance and a new allergen-specific immunotherapy for overcoming problems with current therapies against life-threatening allergic reactions, including anaphylaxis.
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Viney, Joanne L., Allan M. Mowat, Jamie M. O’Malley, Eilidh Williamson, and Neil A. Fanger. "Expanding Dendritic Cells In Vivo Enhances the Induction of Oral Tolerance." Journal of Immunology 160, no. 12 (1998): 5815–25. http://dx.doi.org/10.4049/jimmunol.160.12.5815.
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Abstract The intestine is under perpetual challenge from both pathogens and essential nutrients, yet the mucosal immune system is able to discriminate effectively between harmful and innocuous Ags. It is likely that this selective immunoregulation is dependent on the nature of the APC at sites where gut Ags are processed and presented. Dendritic cells (DC) are considered the most potent of APC and are renowned for their immunostimulatory role in the initiation of immune responses. To investigate the role of DC in regulating the homeostatic balance between mucosal immunity and tolerance, we treated mice with Flt3 ligand (Flt3L), a growth factor that expands DC in vivo, and assessed subsequent systemic immune responsiveness using mouse models of oral tolerance. Surprisingly, mice treated with Flt3L to expand DC exhibited more profound systemic tolerance after they were fed soluble Ag. Most notably, tolerance could be induced in Flt3L-treated mice using very low doses of Ag that were ineffective in control animals. These findings contrast with the generally accepted view of DC as immunostimulatory APC and furthermore suggest a pivotal role for DC during the induction of tolerance following mucosal administration of Ag.
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Zhang, Xiuyuan, Shan Gao, Jinfeng Niu, et al. "Cannabinoid 2 Receptor Agonist Improves Systemic Sensitivity to Insulin in High-Fat Diet/Streptozotocin-Induced Diabetic Mice." Cellular Physiology and Biochemistry 40, no. 5 (2016): 1175–85. http://dx.doi.org/10.1159/000453171.
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Background/Aims: The endocannabinoid signalling (ECS) system has been known to regulate glucose homeostasis. Previous studies have suggested that the cannabinoid 2 (CB2) receptor may play a regulatory role on insulin secretion, immune modulation and insulin resistance. Given that diabetes and insulin resistance are attributable to elevated inflammatory tone, we investigated the role of CB2 receptor on glucose tolerance and insulin sensitivity in high-fat diet (HFD)/streptozotocin (STZ)-induced mice. Methods: Diabetes was induced in male ICR mice by HFD/STZ and exposed to a CB2 receptor agonist, SER601, for 2- or 4-weeks via subcutaneous implantation of osmotic minipumps. Glucose and insulin tolerance tests were performed at the end of treatment. Islets were isolated for assessment of β-cell function. Pancreases and skeletal muscles were also obtained for histological analyses. Results: Despite a lack of impact on glucose tolerance, substantial improvement on insulin sensitivity was observed in SER601-treated mice, which could partly be attributed to improved islet β-cell function, shown as increased glucose-induced insulin secretion and insulin content. No changes on islet macrophage infiltration or skeletal muscle fat deposition were detectable from SER601-treated mice. However, a major decrease in body weight was recorded at the end of 4-week SER601 exposure, accompanied by a lack of epididymal adipose mass in SER601-treated mice. Conclusion: Our data suggest a lipolytic role of SER601 in HFD/STZ-induced diabetic mice, which results in significant improvement of systemic insulin sensitivity. Thus, the CB2 receptor may be considered a promising target for therapeutic development against insulin resistance and obesity-related diabetes.
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Torkzaban, Parviz, and Amir Talaie. "Drug-Induced Gingival Overgrowth in an 8-Year-Old Girl: A Case Report." Avicenna Journal of Dental Research 13, no. 3 (2021): 109–12. http://dx.doi.org/10.34172/ajdr.2021.21.
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Systemic lupus erythematosus is a systemic autoimmune disease that involves multi organs. Genetic, endocrine, immunological, and environmental factors influence the loss of immunological tolerance against self-antigens leading to the formation of pathogenic autoantibodies that cause tissue damage through multiple mechanisms. The gingival overgrowth can be caused by three factors: noninflammatory, hyperplastic reaction to the medication; chronic inflammatory hyperplasia; or a combined enlargement due to chronic inflammation and drug-induced hyperplasia. Drug-Induced Gingival Overgrowth is associated with the use of three major classes of drugs, namely anticonvulsants, calcium channel blockers, and immunosuppressants. Due to recent indications for these drugs, their use continues to grow.
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Mardare, Cornelia, Karsten Krüger, Gerhard Liebisch, et al. "Endurance and Resistance Training Affect High Fat Diet-Induced Increase of Ceramides, Inflammasome Expression, and Systemic Inflammation in Mice." Journal of Diabetes Research 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4536470.
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The study aimed to investigate the effects of differentiated exercise regimes on high fat-induced metabolic and inflammatory pathways. Mice were fed a standard diet (ST) or a high fat diet (HFD) and subjected to regular endurance training (ET) or resistance training (RT). After 10 weeks body weight, glucose tolerance, fatty acids (FAs), circulating ceramides, cytokines, and immunological mediators were determined. The HFD induced a significant increase in body weight and a disturbed glucose tolerance (p<0.05). An increase of plasma FA, ceramides, and inflammatory mediators in adipose tissue and serum was found (p<0.05). Both endurance and resistance training decreased body weight (p<0.05) and reduced serum ceramides (p<0.005). While RT attenuated the increase of NLRP-3 (RT) expression in adipose tissue, ET was effective in reducing TNF-αand IL-18 expression. Furthermore, ET reduced levels of MIP-1γ, while RT decreased levels of IL-18, MIP-1γ, Timp-1, and CD40 in serum (p<0.001), respectively. Although both exercise regimes improved glucose tolerance (p<0.001), ET was more effective than RT. These results suggest that exercise improves HFD-induced complications possibly through a reduction of ceramides, the reduction of inflammasome activation in adipose tissues, and a systemic downregulation of inflammatory cytokines.
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Cheng, Fei, Min Gao, Junyang Lu, Yuan Huang, and Zhilong Bie. "Spatial–Temporal Response of Reactive Oxygen Species and Salicylic Acid Suggest Their Interaction in Pumpkin Rootstock-Induced Chilling Tolerance in Watermelon Plants." Antioxidants 10, no. 12 (2021): 2024. http://dx.doi.org/10.3390/antiox10122024.
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Grafting with pumpkin rootstock could improve chilling tolerance in watermelon, and salicylic acid (SA) as a signal molecule is involved in regulating plant tolerance to chilling and other abiotic stresses. To clarify the mechanism in pumpkin rootstock-induced systemic acquired acclimation in grafted watermelon under chilling stress, we used self-grafted (Cl/Cl) and pumpkin rootstock-grafted (Cl/Cm) watermelon seedlings to study the changes in lipid peroxidation, photosystem II (PSII) activity and antioxidant metabolism, the spatio–temporal response of SA biosynthesis and H2O2 accumulation to chilling, and the role of H2O2 signal in SA-induced chilling tolerance in grafted watermelon. The results showed that pumpkin rootstock grafting promoted SA biosynthesis in the watermelon scions. Chilling induced hydrolysis of conjugated SA into free SA in the roots and accumulation of free SA in the leaves in Cl/Cm plants. Further, pumpkin rootstock grafting induced early response of antioxidant enzyme system in the roots and increased activities of ascorbate peroxidase and glutathione reductase in the leaves, thus maintaining cellular redox homeostasis. Exogenous SA improved while the inhibition of SA biosynthesis reduced chilling tolerance in Cl/Cl seedlings. The application of diphenyleneiodonium (DPI, inhibitor of NADPH oxidase) and dimethylthiourea (DMTU, H2O2 scavenger) decreased, while exogenous H2O2 improved the PSII activity in Cl/Cl plants under chilling stress. Additionally, the decrease of the net photosynthetic rate in DMTU- and DPI-pretreated Cl/Cl plants under chilling conditions could be alleviated by subsequent application of H2O2 but not SA. In conclusion, pumpkin rootstock grafting induces SA biosynthesis and redistribution in the leaves and roots and participates in the regulation of antioxidant metabolism probably through interaction with the H2O2 signal, thus improving chilling tolerance in watermelon.
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Gangur, Venu. "A mouse model of food induced acute allergic angioedema (141.10)." Journal of Immunology 184, no. 1_Supplement (2010): 141.10. http://dx.doi.org/10.4049/jimmunol.184.supp.141.10.
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Abstract Previous studies report that without the use of adjuvant such as cholera toxin, oral exposure to peanut proteins in mice results in oral tolerance. Here we tested the hypothesis that oral administration of peanut butter (instead of soluble peanut proteins) would be sufficient to sensitize C3H/Hej mice for peanut allergy. Groups of C3H/Hej mice were exposed to peanut butter or saline (orally, once per week) and examined for systemic IgE and IgG1 responses. Oral administration of peanut butter, but not saline, resulted in systemic peanut specific IgG1 and IgE antibody responses. Notably, as little as two oral exposures to peanut butter resulted in dramatic IgG1 antibody responses. Peanut butter elicited IgE and IgG1 antibodies were able to bind to peanut protein extract as well as to peanut butter preparation in ELISA system. Furthermore, oral challenge of sensitized mice, but not saline control mice, with peanut butter resulted in clinical symptoms of acute allergic angioedema with swollen lips, nostrils, face and eyelids. Mice also exhibited itching-scratching and rubbing symptoms with abnormal breathing. These data demonstrate for the first time that: oral peanut butter administration to C3H/Hej mice does not result in oral tolerance, but instead results in clinical sensitization for acute allergic angioedema. Funding: US EPA STAR Grant#R833133
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Gesualdo, L., M. E. Lamm, and S. N. Emancipator. "Defective oral tolerance promotes nephritogenesis in experimental IgA nephropathy induced by oral immunization." Journal of Immunology 145, no. 11 (1990): 3684–91. http://dx.doi.org/10.4049/jimmunol.145.11.3684.
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Abstract Oral tolerance, an important feature of the mucosal immune system, appears to protect against immune-mediated disease by blunting production of systemic IgG and IgM antibody directed toward immunogens chronically present at mucosal surfaces. In this study, we explored the role of oral tolerance and mucosal immunoregulation in an experimental model of IgA nephropathy (IgAN), an important form of nephritis in humans. Cyclophosphamide and estradiol were used to inhibit the expression of oral tolerance, which otherwise develops after chronic oral presentation of Ag. BALB/c mice given drinking water containing 0.1% bovine gamma globulin (BGG) continuously for 14 wk were randomly assigned to groups given either 2 mg of cyclophosphamide i.p., 2 mg of estradiol s.c. or both drugs. Groups of control mice received neither BGG nor drugs. In three separate experiments, a low percentage of saline-treated orally immunized mice had microscopic hematuria (0 to 20%), as did nonimmunized controls (0 to 20%). However, 58 to 83% of mice given estradiol and/or cyclophosphamide at appropriate times developed significant hematuria. If drugs were given at suboptimal times, only 25 to 56% of mice developed hematuria. Drug-treated immunized mice also had more serum IgG and IgM anti-BGG antibodies than control and saline groups. Immunofluorescence showed significantly more glomerular deposits of IgG, IgM, and C3 in drug-treated immunized mice compared to saline-treated immunized and normal untreated control mice. Hematuria and glomerular deposits of IgG, IgM, and C3 paralleled serum IgG and IgM antibody. All immunized mice showed significant mesangial IgA and BGG deposits and there were no differences in such deposits between saline- and drug-treated immunized mice. We suggest that blunting of oral tolerance with promotion of systemic IgG and IgM antibody production leads to nephritis in chronically orally immunized mice and that glomerular immune complexes containing IgG and/or IgM promote complement deposition and hematuria in IgAN. Analogous defects in oral (or more generally mucosal) tolerance could play a role in the genesis of symptomatic human IgAN.
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Hecker, Peter A., Rudo F. Mapanga, Charlene P. Kimar, et al. "Effects of glucose-6-phosphate dehydrogenase deficiency on the metabolic and cardiac responses to obesogenic or high-fructose diets." American Journal of Physiology-Endocrinology and Metabolism 303, no. 8 (2012): E959—E972. http://dx.doi.org/10.1152/ajpendo.00202.2012.
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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common human enzymopathy that affects cellular redox status and may lower flux into nonoxidative pathways of glucose metabolism. Oxidative stress may worsen systemic glucose tolerance and cardiometabolic syndrome. We hypothesized that G6PD deficiency exacerbates diet-induced systemic metabolic dysfunction by increasing oxidative stress but in myocardium prevents diet-induced oxidative stress and pathology. WT and G6PD-deficient (G6PDX) mice received a standard high-starch diet, a high-fat/high-sucrose diet to induce obesity (DIO), or a high-fructose diet. After 31 wk, DIO increased adipose and body mass compared with the high-starch diet but to a greater extent in G6PDX than WT mice (24 and 20% lower, respectively). Serum free fatty acids were increased by 77% and triglycerides by 90% in G6PDX mice, but not in WT mice, by DIO and high-fructose intake. G6PD deficiency did not affect glucose tolerance or the increased insulin levels seen in WT mice. There was no diet-induced hypertension or cardiac dysfunction in either mouse strain. However, G6PD deficiency increased aconitase activity by 42% and blunted markers of nonoxidative glucose pathway activation in myocardium, including the hexosamine biosynthetic pathway activation and advanced glycation end product formation. These results reveal a complex interplay between diet-induced metabolic effects and G6PD deficiency, where G6PD deficiency decreases weight gain and hyperinsulinemia with DIO, but elevates serum free fatty acids, without affecting glucose tolerance. On the other hand, it modestly suppressed indexes of glucose flux into nonoxidative pathways in myocardium, suggesting potential protective effects.
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Uknes, S., T. Delaney, B. Vernooij, et al. "1007 SYSTEMIC ACQUIRED RESISTANCE." HortScience 29, no. 5 (1994): 573g—574. http://dx.doi.org/10.21273/hortsci.29.5.573g.
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Systemic acquired resistance is a broad spectrum inducible defense response that is associated with the expression of a set of genes (SAR genes). Expression of one of these genes (PR-1a from tobacco) in transgenic tobacco confers increased tolerance to two oomycete pathogens. A direct role for salicylic acid (SA) in signaling SAR has been established in tobacco by analysis of transgenic tobacco expressing salicylate hydroxylase (SAH, an enzyme that inactivates SA by conversion to catechol). Tobacco plants that express SAH are blocked in the accumulation of SA and the development of SAR when responding lo TMV. Furthermore, both Arabidopsis and tobacco expressing SAH have altered pathogen induced lesion morphology, exemplified by larger spreading lesions. Putative mutants in SAR gene expression were isolated by screening M2 Arabidopsis plants for altered expression of PR-1 and PR-2 or for sensitivity to pathogen infection following INA treatment. The putative mutants all into two major classes,constitutive (cim, constitutive immunity) and non-inducible (nim, non-inducible immunity). Several cim mutants exhibits a disease lesion phenotype in the absence of pathogen.
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Han, Qiuju, Peixiang Lan, Jian Zhang, Cai Zhang, and Zhigang Tian. "Reversal of hepatitis B virus-induced systemic immune tolerance by intrinsic innate immune stimulation." Journal of Gastroenterology and Hepatology 28 (July 15, 2013): 132–37. http://dx.doi.org/10.1111/jgh.12034.
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Zhou, Yufeng, Hirokazu Kawasaki, Shih-Chang Hsu, et al. "Oral tolerance to food-induced systemic anaphylaxis mediated by the C-type lectin SIGNR1." Nature Medicine 16, no. 10 (2010): 1128–33. http://dx.doi.org/10.1038/nm.2201.
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Seidel-Guyenot, Wolfgang, Sylwia Perschon, Natascha Dechant, Ruth Alt, Jürgen Knop, and Kerstin Steinbrink. "Low zone tolerance induced by systemic application of allergens inhibits TC1-mediated skin inflammation." Journal of Allergy and Clinical Immunology 117, no. 5 (2006): 1170–77. http://dx.doi.org/10.1016/j.jaci.2006.01.014.
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Weaver, Kourtney D., Liz Simon, Patricia E. Molina, and Flavia Souza-Smith. "The Role of Lymph-Adipose Crosstalk in Alcohol-Induced Perilymphatic Adipose Tissue Dysfunction." International Journal of Molecular Sciences 25, no. 19 (2024): 10811. http://dx.doi.org/10.3390/ijms251910811.
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Chronic alcohol use leads to metabolic dysfunction in adipose tissue. The underlying mechanisms and the contribution of alcohol-induced adipose tissue dysfunction to systemic metabolic dysregulation are not well understood. In our previous studies, we found that chronic alcohol feeding induces mesenteric lymphatic leakage, perilymphatic adipose tissue (PLAT) inflammation, and local insulin resistance in rats. The goal of this study was to further explore the link between alcohol-induced lymphatic leakage and PLAT immunometabolic dysregulation, locally and systemically, using in vivo and ex vivo approaches. Male rats received a Lieber–DeCarli liquid diet, of which 36% of the calories were from alcohol, for 10 weeks. Time-matched control animals were pair-fed. Adipokine levels were measured in PLAT, subcutaneous fat, plasma, and mesenteric lymph samples. Glucose tolerance was assessed after 10 weeks. Further, we used a novel ex vivo lymph-stimulated naïve PLAT explant approach to modeling lymph leakage to assess changes in adipokine secretion and expression of proinflammatory markers after stimulation with lymph from alcohol- or pair-fed animals. Our data show that chronic alcohol-fed rats presented PLAT-specific decreases in adiponectin and leptin levels, alterations in the expression of genes involved in lipid metabolic pathways, and associated impaired whole-body glucose homeostasis. Further, we found that direct naïve PLAT stimulation with lymph contents from alcohol-fed animals increased IL-6 expression in demonstrating the ability of lymph contents to differentially impact naïve adipose tissue. Overall, chronic alcohol feeding leads to depot-specific alterations in metabolic profile, impaired systemic glucose tolerance, and lymph-induced adipose tissue inflammation. The specific lymph components leading to PLAT immunometabolic dysregulation remain to be determined.
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Young, Kevin J., Liming Yang, M. James Phillips, and Li Zhang. "Donor-lymphocyte infusion induces transplantation tolerance by activating systemic and graft-infiltrating double-negative regulatory T cells." Blood 100, no. 9 (2002): 3408–14. http://dx.doi.org/10.1182/blood-2002-01-0235.
Full textAbstract:
Abstract Donor-lymphocyte infusion (DLI) before transplantation can lead to specific tolerance to allografts in mice, nonhuman primates, and humans. We and others have demonstrated a role for regulatory T cells in DLI-induced, donor-specific transplantation tolerance, but it is not known how regulatory T cells are activated and where they execute their function. In this study, we observed, in both transgenic and normal mice, that DLI before transplantation is required for activation of αβ-T-cell-receptor–positive, CD3+CD4−CD8− double-negative (DN) regulatory T cells in the periphery of recipient mice. More interestingly, DLI induced DN regulatory T cells to migrate preferentially to donor-specific allogeneic skin grafts and to form a majority of graft-infiltrating T cells in accepted skin allografts. Furthermore, both recipient-derived peripheral and graft-infiltrating DN T cells were able to suppress and kill antidonor CD8+ T cells in an antigen-specific manner. These data indicate that DLI may induce donor-specific transplantation tolerance by activating recipient DN regulatory T cells in the periphery and by promoting migration of regulatory T cells to donor-specific allogeneic skin grafts. Our results also show that DN regulatory T cells can eliminate antidonor T cells both systemically and locally, a finding suggesting that graft-infiltrating T cells can be beneficial to graft survival.
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Worbs, Tim, Ulrike Bode, Sheng Yan, et al. "Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells." Journal of Experimental Medicine 203, no. 3 (2006): 519–27. http://dx.doi.org/10.1084/jem.20052016.
Full textAbstract:
Oral tolerance induction is a key feature of intestinal immunity, generating systemic nonresponsiveness to ingested antigens. In this study, we report that orally applied soluble antigens are exclusively recognized in the intestinal immune system, particularly in the mesenteric lymph nodes. Consequently, the initiation of oral tolerance is impeded by mesenteric lymphadenectomy. Small bowel transplantation reveals that mesenteric lymph nodes require afferent lymph to accomplish the recognition of orally applied antigens. Finally, oral tolerance cannot be induced in CCR7-deficient mice that display impaired migration of dendritic cells from the intestine to the mesenteric lymph nodes, suggesting that immunologically relevant antigen is transported in a cell-bound fashion. These results demonstrate that antigen transport via afferent lymphatics into the draining mesenteric lymph nodes is obligatory for oral tolerance induction, inspiring new therapeutic strategies to exploit oral tolerance induction for the prevention and treatment of autoimmune diseases.
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Collins, L. Vincent, Kristina Eriksson, Robert G. Ulrich, and Andrej Tarkowski. "Mucosal Tolerance to a Bacterial Superantigen Indicates a Novel Pathway To Prevent Toxic Shock." Infection and Immunity 70, no. 5 (2002): 2282–87. http://dx.doi.org/10.1128/iai.70.5.2282-2287.2002.
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ABSTRACT Enterotoxins with superantigenic properties secreted during systemic Staphylococcus aureus infection are responsible for toxic shock. We show that intranasal administration of staphylococcal enterotoxin A (SEA), but not a recombinant SEA lacking superantigenic activity, protected mice against lethal systemic SEA challenge. Protection was superantigen specific since intranasal exposure to SEA would not protect against death caused by subsequent toxic shock syndrome toxin 1 systemic challenge. Protection was neither due to selective depletion of SEA-specific T-cell receptor Vβ families nor due to production of neutralizing anti-SEA antibodies. Importantly, the production of interleukin 10 (IL-10) induced by “tolerization” (that is, by the induction of immunological tolerance) contributed to the observed protection against lethal superantigen-triggered disease. In support of this notion we found that (i) significantly increased levels of IL-10 in sera of “tolerized” animals (that is, animals rendered tolerant) and (ii) IL-10−/− mice could not be tolerized by mucosal SEA administration. Altogether, this is the first study to show that mucosal tolerance to a superantigen is readily triggered by means of immunodeviation.
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Jha, Prabhat N., Garima Gupta, Prameela Jha, and Rajesh Mehrotra. "Association of Rhizospheric/Endophytic Bacteria with Plants: A Potential Gateway to Sustainable Agriculture." Greener Journal of Agricultural Sciences 3, no. 2 (2013): 073–84. https://doi.org/10.15580/GJAS.2013.2.010313354.
Full textAbstract:
<strong>Application of associative bacteria for sustainable agriculture holds immense potential. These bacteria are known to enhance growth and yield of plants by fixing atmospheric nitrogen, solubilization of phosphate, production of phytohormones and siderophores, possession of antagonistic activity as well as reducing the level of stress ethylene in host plants. Colonization of these bacteria can be tracked by tagg</strong><strong>ing them with certain molecular markers such as β-glucuronidase (</strong><strong><em>gus</em></strong><strong>) or green fluorescent protein (</strong><strong><em>gfp</em></strong><strong>) followed by electron microscopy or laser scanning confocal microscopy. Associative bacteria and endophytes may express genes differentially to colonize and establish the plant interior. They may also use ‘quorum sensing’ molecules for colonization process. Present review aims to highlight various plant growth promoting properties, ecology and updates of molecular mechanisms involved in interaction between associative bacteria and plants as well as immune responses triggered by these bacteria in plants</strong><strong>.</strong>