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Relevant bibliographies by topics / T cells. Suppressor cells. Immunological tolerance

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Academic literature on the topic 'T cells. Suppressor cells. Immunological tolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "T cells. Suppressor cells. Immunological tolerance"

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Nakamura, Tsukasa, and Hidetaka Ushigome. "Myeloid-Derived Suppressor Cells as a Regulator of Immunity in Organ Transplantation." International Journal of Molecular Sciences 19, no. 8 (August 10, 2018): 2357. http://dx.doi.org/10.3390/ijms19082357.

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Regulation of allo-immune responses is proposed as a topic for investigation in the current field of organ transplantation. As a regulator, regulatory T cells (Tregs) have received attention due to their ability to control allograft rejection. Concurrently, however, the independent action of Tregs is not enough to achieve tolerance status in many situations. Meanwhile, as a multi-functional regulator, myeloid-derived suppressor cells (MDSCs) can suppress effector T cells as well as induce Tregs or regulatory B cells (Bregs) in certain circumstances. Furthermore, the importance of a crosstalk between MDSCs and natural killer T cells to induce tolerance has been reported. Thus, orchestration between MDSCs, myeloid regulators, T/Bregs and other lymphoid/myeloid regulators can shed light on achieving allogeneic tolerance. Here, we review the current knowledge in terms of immunological regulatory function displayed by MDSCs in the context of organ transplantation. Ideal control of MDSCs would lead to a reduction of allograft rejection and subsequent long-term allograft acceptance.

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Apostolou, Irina, and Harald von Boehmer. "In Vivo Instruction of Suppressor Commitment in Naive T Cells." Journal of Experimental Medicine 199, no. 10 (May 17, 2004): 1401–8. http://dx.doi.org/10.1084/jem.20040249.

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The induction of antigen-specific tolerance in the mature immune system of the intact organism has met with limited success. Therefore, nonspecific immunosuppression has been the treatment of choice to prevent unwanted immunity. Here, it is shown that prolonged subcutaneous infusion of low doses of peptide by means of osmotic pumps transforms mature T cells into CD4+25+ suppressor cells that can persist for long periods of time in the absence of antigen and confer specific immunologic tolerance upon challenge with antigen. The described procedure resembles approaches of tolerance induction used decades ago, induces tolerance in the absence of immunity, and holds the promise to become an effective means of inducing antigen-specific tolerance prospectively, whereas its power to suppress already ongoing immune responses remains to be determined.

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Chen, WanJun, Wenwen Jin, Neil Hardegen, Ke-jian Lei, Li Li, Nancy Marinos, George McGrady, and Sharon M. Wahl. "Conversion of Peripheral CD4+CD25− Naive T Cells to CD4+CD25+ Regulatory T Cells by TGF-β Induction of Transcription Factor Foxp3." Journal of Experimental Medicine 198, no. 12 (December 15, 2003): 1875–86. http://dx.doi.org/10.1084/jem.20030152.

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CD4+CD25+ regulatory T cells (Treg) are instrumental in the maintenance of immunological tolerance. One critical question is whether Treg can only be generated in the thymus or can differentiate from peripheral CD4+CD25− naive T cells. In this paper, we present novel evidence that conversion of naive peripheral CD4+CD25− T cells into anergic/suppressor cells that are CD25+, CD45RB−/low and intracellular CTLA-4+ can be achieved through costimulation with T cell receptors (TCRs) and transforming growth factor β (TGF-β). Although transcription factor Foxp3 has been shown recently to be associated with the development of Treg, the physiological inducers for Foxp3 gene expression remain a mystery. TGF-β induced Foxp3 gene expression in TCR-challenged CD4+CD25− naive T cells, which mediated their transition toward a regulatory T cell phenotype with potent immunosuppressive potential. These converted anergic/suppressor cells are not only unresponsive to TCR stimulation and produce neither T helper cell 1 nor T helper cell 2 cytokines but they also express TGF-β and inhibit normal T cell proliferation in vitro. More importantly, in an ovalbumin peptide TCR transgenic adoptive transfer model, TGF-β–converted transgenic CD4+CD25+ suppressor cells proliferated in response to immunization and inhibited antigen-specific naive CD4+ T cell expansion in vivo. Finally, in a murine asthma model, coadministration of these TGF-β–induced suppressor T cells prevented house dust mite–induced allergic pathogenesis in lungs.

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Wang, Dangge, Tingting Wang, Haijun Yu, Bing Feng, Lei Zhou, Fangyuan Zhou, Bo Hou, Hanwu Zhang, Min Luo, and Yaping Li. "Engineering nanoparticles to locally activate T cells in the tumor microenvironment." Science Immunology 4, no. 37 (July 12, 2019): eaau6584. http://dx.doi.org/10.1126/sciimmunol.aau6584.

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Immunological tolerance of tumors is characterized by insufficient infiltration of cytotoxic T lymphocytes (CTLs) and immunosuppressive microenvironment of tumor. Tumor resistance to immune checkpoint inhibitors due to immunological tolerance is an ongoing challenge for current immune checkpoint blockade (ICB) therapy. Here, we report the development of tumor microenvironment–activatable anti-PDL1 antibody (αPDL1) nanoparticles for combination immunotherapy designed to overcome immunological tolerance of tumors. Combination of αPDL1 nanoparticle treatment with near-infrared (NIR) laser irradiation–triggered activation of photosensitizer indocyanine green induces the generation of reactive oxygen species, which promotes the intratumoral infiltration of CTLs and sensitizes the tumors to PDL1 blockade therapy. We showed that the combination of antibody nanoparticles and NIR laser irradiation effectively suppressed tumor growth and metastasis to the lung and lymph nodes in mouse models. The nanoplatform that uses the antibody nanoparticle alone both for immune stimulation and PDL1 inhibition could be readily adapted to other immune checkpoint inhibitors for improved ICB therapy.

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Shakhov, A. G., S. V. Shabunin, L. Yu Sashnina, M. I. Adodina, M. Yu Zhejnes, K. V. Tarakanova, and K. O. Kopytina. "CELLULAR IMMUNITY AND CYTOKINE PROFILE IN PRE-FARROW AND LACTATING SOWS." Veterinary Science Today, no. 3 (October 3, 2019): 15–22. http://dx.doi.org/10.29326/2304-196x-2019-3-30-15-18.

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Study results of cellular immunity and cytokine profile of commercial pre-farrow and lactating sows are shown. Before farrow, the animals demonstrated physiological immunodeficiency characterized by relative leukopenia and lymphopenia, decreased T-cell number, higher helper/suppressor ratio providing immunological tolerance in dam/fetus system. Their cytokine profile was specified by relatively deficient interleukin-1β and tumor necrosis factor-α indicative of immune system suppression and high level of γ-interferon involved in parturition and activation of suppressor cells. Post-farrow sows demonstrated higher cellular immunity involving higher levels of leukocytes, lymphocytes and T-cells as well as tendency of T-lymphocyte helper/suppressor ratio reduction being indicative of T-cells’ suppressor activity. The cytokine profile of the sows was specified by the recovered numbers of interleukin-1β, tumor necrosis factor-α and γ-interferon, decreased level of interleukin-2 and interleukin-4 that regulate cellular and humoral immunity, respectively as well as their subsequent increase (in particular, interleukin-2) following animal immunization against parvoviral infection and erysipelas on day 7 post farrowing (Parvoruvax vaccine, Merial, France) and against classical swine fever on day 14 post farrowing (culture dry virus-vaccine LK-VNIVIPFIT). This is due to the formation of the cellular and humoral immunity.

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Steinbrink, K., C. Sorg, and E. Macher. "Low zone tolerance to contact allergens in mice: a functional role for CD8+ T helper type 2 cells." Journal of Experimental Medicine 183, no. 3 (March 1, 1996): 759–68. http://dx.doi.org/10.1084/jem.183.3.759.

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Normal skin is permeable to low molecular hydrophobic substances, including allergenic chemicals. Whereas such foreign matter appears to enter the skin naturally, it rarely induces contact hypersensitivity. This suggests that immunological tolerance would be the normal state of affairs. In search of a suitable model, we painted picryl chloride or oxazolone once or repeatedly on normal skin of BALB/c or C57B1/6 mice and found subsensitizing doses to be tolerogenic. The most effective doses in inducing tolerance were doses between those at the point of inflection from no responses to threshold sensitivity. But even doses three orders of magnitude lower than these suppressed subsequent sensitization if applied repeatedly. C57B1/6 mice (low responders) were consistently easier to make tolerant than BALB/c mice (high responders). The tolerant state established by a single painting was found to be fully developed at 48 h after initiation and long-lasting (>14 d). It could be adoptively transferred by intravenous injection of total spleen cells (SC), lymph node cells (LNC), or purified T cells and shown to be hapten specific. Pretreatment with cyclophosphamide (Cy) prevented tolerization. The T cells capable of transferring suppressive activity were found to be generated irrespective of the dose applied. On day 2 after painting, tolerance could be transferred with LNC from both tolerant and sensitized animals. On day 5, however, only cells from tolerant donors transferred tolerance. But by action of Cy, suppression was shown to be part of every sensitization, although masked. Production of hapten-specific antibodies was suppressed as well. Through depletion by monoclonal antibody in vitro the T suppressor cells were shown to belong to the murine CD8+ subset (Lyt2+). Upon restimulation in vitro by haptenized and irradiated normal SC, LNC from tolerant donors produced predominantly interleukin (IL)-4, IL-5, and IL-10. In contrast, LNC from sensitized donors produced preferentially IL-2 and interferon-gamma. Thus we demonstrate that painting subsensitizing doses of contact sensitizers on normal murine skin generates CD8+ Th2-like cells that give rise to hapten-specific tolerance. The model may have broader significance and apply to other species, including humans.

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Gonzalez-Rey, E., M. A. Gonzalez, N. Varela, F. O’Valle, P. Hernandez-Cortes, L. Rico, D. Büscher, and M. Delgado. "Human adipose-derived mesenchymal stem cells reduce inflammatory and T cell responses and induce regulatory T cells in vitro in rheumatoid arthritis." Annals of the Rheumatic Diseases 69, no. 01 (January 5, 2009): 241–48. http://dx.doi.org/10.1136/ard.2008.101881.

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Objectives:Adult mesenchymal stem cells were recently found to suppress effector T cell and inflammatory responses and have emerged as attractive therapeutic candidates for immune disorders. In rheumatoid arthritis (RA), a loss in the immunological self-tolerance causes the activation of autoreactive T cells against joint components and subsequent chronic inflammation. The aim of this study is to characterise the immunosuppressive activity of human adipose-derived mesenchymal stem cells (hASCs) on collagen-reactive T cells from patients with RA.Methods:The effects of hASCs on collagen-reactive RA human T cell proliferation and cytokine production were investigated, as well as effects on the production of inflammatory mediators by monocytes and fibroblast-like synoviocytes from patients with RA.Results:hASCs suppressed the antigen-specific response of T cells from patients with RA. hASCs inhibited the proliferative response and the production of inflammatory cytokines by collagen-activated CD4 and CD8 T cells. In contrast, the numbers of IL10-producing T cells and monocytes were significantly augmented upon hASC treatment. The suppressive activity of hASCs was cell-to-cell contact dependent and independent. hASCs also stimulated the generation of FoxP3 protein-expressing CD4+CD25+ regulatory T cells, with the capacity to suppress collagen-specific T cell responses. Finally, hASCs downregulated the inflammatory response and the production of matrix-degrading enzymes by synovial cells isolated from patients with RA.Conclusions:The present work identifies hASCs as key regulators of immune tolerance, with the capacity to suppress T cell and inflammatory responses and to induce the generation/activation of antigen-specific regulatory T cells.

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Pilat, Nina, Benedikt Mahr, Martina Gattringer, Ulrike Baranyi, and Thomas Wekerle. "CTLA4Ig Improves Murine iTreg Induction via TGFβ and Suppressor Function In Vitro." Journal of Immunology Research 2018 (July 2, 2018): 1–10. http://dx.doi.org/10.1155/2018/2484825.

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Blockade of the CD28:CD80/86 costimulatory pathway has been shown to be potent in blocking T cell activation in vitro and in vivo. The costimulation blocker CTLA4Ig has been approved for the treatment of autoimmune diseases and transplant rejection. The therapeutic application of regulatory T cells (Tregs) has recently gained much attention for its potential of improving allograft survival. However, neither costimulation blockade with CTLA4Ig nor Treg therapy induces robust tolerance on its own. Combining CTLA4Ig with Treg therapy would be an attractive approach for minimizing immunosuppression or for possibly achieving tolerance. However, since the CD28 pathway is more complex than initially thought, the question arose whether blocking CD80/86 would inadvertently impact immunological tolerance by interfering with Treg generation and function. We therefore wanted to investigate the compatibility of CTLA4Ig with regulatory T cells by evaluating direct effects of CTLA4Ig on murine Treg generation and function in vitro. For generation of polyclonal-induced Tregs, we utilized an APC-free in vitro system and added titrated doses of CTLA4Ig at different time points. Phenotypical characterization by flow cytometry and functional characterization in suppressor assays did not reveal negative effects by CTLA4Ig. The costimulation blocker CTLA4Ig does not impair but rather improves murine iTreg generation and suppressor function in vitro.

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Miner, Samantha, Nancy F. Hensel, Bahey Salem, Neil Dunavin, Kazushi Tanimoto, Minoo Battiwalla, Kit Lu, et al. "A Novel Standardized Quantitative Suppression Assay Reveals a Diversity of Human Immune-Regulatory Cell Potency." Blood 124, no. 21 (December 6, 2014): 316. http://dx.doi.org/10.1182/blood.v124.21.316.316.

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Abstract Immunologic tolerance is a critical homeostatic function to protect self from auto-immunity. Various immune-regulatory cells, including regulatory T cell (Treg), myeloid derived suppressor cell (MDSC), tolerogenic dendritic cell, and mesenchymal stromal cell (MSC) are responsible for orchestrating this tolerance. Immune-regulatory cells play a central role in the pathophysiology of cancer immunity, autoimmune disease, and graft versus host disease and can be used in adoptive cell therapy. There is therefore a need for a standardized method to evaluate the suppressive function of these heterogeneous cell populations. We developed an in vitro standardized quantitative suppression assay utilizing the suppressor cell line KARPAS-299 as a standard by which to compare suppressive potency of human immune-regulatory cell populations. Peripheral CD4 T-cells, used as targets in all assays, were isolated from healthy donors (n=30) using an automated cell separator or by flow sorting. After labeling with Cell Tracer Violet (CTV), CD4 T-cells were co-cultured with immune-regulatory cells such as autologous Treg, autologous or third party MDSC (CD11b+CD14+), third party bone marrow derived MSC, and primary leukemia cells, or with the reference KARPAS-299 cells. After stimulating with CD3/CD28 beads, CD154 activation of CD4 T-cells was measured at 16 hours, and CD4 T-cell proliferation was measured by CTV dilution within the viable cell population at 72 hours. Suppressive capacities of immune-regulatory cell types were represented as KARPAS-299 suppressor units (KSU), calculated using the equation b/a, where b is the percentage of suppression in the presence of a given immune-regulatory cell, and a is the percentage of suppression in the presence of KARPAS-299. KARPAS-299 cells reproducibly suppressed healthy donor CD4 T-cells at suppressor: responder ratio of 4:1 for both CD154 activation (percentage of suppression 46.2±18.8%) and proliferation (51.0±20.7%). Immune-regulatory cells showed diverse suppressive capacities: autologous MDSC (63.2±24.5%), allogeneic MDSC (55.8±21.8%), third party MSC (51.26±23.67%), and autologous Treg, (8.7±10.4%). After standardization with KSU, MDSC and MSC showed significantly higher suppressive capacity compared to Treg (MDSC 1.18±0.6 KSU, MSC 1.3±1.11 KSU, Treg 0.15±0.3 KSU: p<0.0001). This standardized assay was also applicable to other types of proliferating targets, such as flow-sorted conventional T cells (Tcon: CD4+CD127highCD25low: 2.73±1.78 KSU with autologous MDSC, 1.6±0.75 KSU with third party MSC) and CD8 T-cells (1.49±0.96 KSU with autologous MDSC, 1.08±0.77 with third party MSC). We validated the method as a potency assay of MSC products, and showed inter-individual differences in MSC. Finally, we used the assay to demonstrate a modest suppressive capacity of acute myeloid leukemia blasts (0.35±0.28 KSU). This method provides a platform for standardizing suppressor function to facilitate comparison between laboratories and for use in cell product release assay. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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Burstein, H. J., and A. K. Abbas. "In vivo role of interleukin 4 in T cell tolerance induced by aqueous protein antigen." Journal of Experimental Medicine 177, no. 2 (February 1, 1993): 457–63. http://dx.doi.org/10.1084/jem.177.2.457.

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High doses of aqueous protein antigens induce a form of immunological tolerance in which interleukin 2 (IL-2)- and interferon gamma (IFN-gamma)-secreting T helper type 1 (Th1) cells are inhibited, but IL-4-secreting (Th2) cells are not. This is manifested by reduced proliferation of antigen-specific T cells upon in vitro restimulation, and marked suppression of specific antibody responses of the immunoglobulin (Ig)G2a, IgG2b, and IgG3 isotypes, but not of IgG1 and IgE. The role of the immunomodulatory cytokine IL-4 in this model of unresponsiveness to protein antigens has been examined. Administration of tolerizing antigen itself primes splenic CD4+ T cells for secretion of lymphokines, both IL-2 and IL-4. Neutralization of IL-4 in vivo with the anti-IL-4 antibody 11B11 during tolerance induction augments IFN-gamma production by T cells of tolerant mice, and reverses the suppression of IgG2a, IgG2b, and IgG3. This blockade of IL-4 function does not, however, restore the proliferative responses of T cells, suggesting that reduced T cell proliferation is due to direct T cell inactivation or anergy. Inhibiting the activity of IL-4 in vivo also inhibits the expansion of antigen-specific Th2-like cells, which are resistant to the induction of unresponsiveness. Thus, the immunologic consequences of high-dose tolerance are due to a combination of clonal T cell anergy and IL-4-mediated immune regulation.

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Dissertations / Theses on the topic "T cells. Suppressor cells. Immunological tolerance"

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Strainic, Michael George Jr. "THE ABSENCE OF C3AR AND C5AR SIGNAL TRANSDUCTION PROMOTES T REGULATORY CELL DIFFERENTIATION AND REGULATES IMMUNOLOGIC TOLERANCE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1363707372.

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Divekar, Rohit Dilip Zaghouani Habib. "Two aspects of peripheral immune tolerance systemic and mucosal tolerance mechanisms /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6868.

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The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on April 1, 2010). Vita. Thesis advisor: Habib Zaghouani. "May 2008" Includes bibliographical references.

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Morton, Angela Mary Young. "Investigation of T cell signalling events regulating immunity and tolerance in vivo." Thesis, Connect to e-thesis, 2008. http://theses.gla.ac.uk/59/.

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Thesis (Ph.D.) - University of Glasgow, 2007.
Ph.D. thesis submitted to the Division of Immunology, Infection and Inflammation, Faculty of Medicine, University of Glasgow, 2007. Includes bibliographical references.

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Allan, Sarah E. "Defining the biological role of FOXP3 in human CD4+ T cells." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1122.

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The involvement of regulatory T cells (Tregs) in immune homeostasis is now recognized as one of the fundamental mechanisms of immune tolerance. While several different types of Tregs cooperate to establish and maintain immune homeostasis, much current research is focused on defining the characteristics of the CD4⁺CD25⁺ Treg subset, as these cells can mediate dominant, long-lasting and transferable tolerance in many experimental models. The aim of this research was to characterize the biological role of a protein known as forkhead box P3 (FOXP3) that was initially identified as an essential transcription factor for the development of mouse CD4⁺CD25⁺ Tregs, in human CD4⁺ T cells. Following confirmation that, like mouse Tregs, human Tregs also expressed high levels of FOXP3, several approaches were used to investigate the role of this protein in human CD4⁺ T cells. 1) Characterization of endogenous FOXP3 expression in CD4⁺ T cell subsets revealed that this protein is not a Treg-specific marker as was previously thought. Instead, low-level and transient expression was found to be typical of highly activated non-regulatory effector T cells. 2) To generate large numbers of Tregs suitable for cellular therapy, the capacity of ectopic FOXP3 expression to drive Treg generation in vitro was explored. It was found that high and constitutive expression mediated by a lentiviral vector, but not fluctuating expression driven by a retroviral vector, was sufficient to generate suppressive cells. Over-expression strategies were also used to characterize a novel splice isoform unique to human cells, FOXP3Δ2 (FOXP3b). 3) To further probe the requirements of FOXP3 to induce suppressor function, a system for conditionally-active FOXP3 ectopic expression was developed. These studies established that FOXP3 acts a quantitative regulator rather than a “master switch” for Tregs, and that there is a temporal component to its capacity to direct Treg phenotype and function. In summary, this research has significantly expanded the understanding of the biological function of FOXP3 in human CD4⁺ T cells. Based on the potential of these cells to be manipulated for therapy, this work contributes to the field of immunology on both academic and clinical research fronts.

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Lute, Kenneth D. "Costimulation and tolerance in T cell immunotherapy." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141850521.

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Ramos, Rodrigo Nalio. "Investigação de um possível viés imunossupressor em células dendríticas derivadas de indivíduos portadores de cancêr." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-12082011-135929/.

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As células dendríticas (DCs) são as mais eficazes células apresentadoras de antígenos. Mesmo com a possibilidade da geração de DCs in vitro, que permitiu a criação de protocolos de vacinação antitumoral, mecanismos de tolerância periférica, mediados por células T reguladoras, impedem uma resposta imune antitumoral eficaz. O presente estudo visou avaliar, in vitro, a geração de linfócitos T reguladores por células dendríticas derivadas de pacientes portadoras de câncer de mama. Para tanto, DCs foram diferenciadas a partir de monócitos do sangue periférico de pacientes com câncer, por sete dias, na presença de GM-CSF e IL-4 (DCs imaturas - iDCs), e ativadas, por adição de TNF-a no dia cinco de cultura (DCs maduras - mDCs). As DCs foram caracterizadas, por citometria de fluxo, quanto à: expressão de CD1a, CD11c, CD14, CD80, CD86, CD83, CD123, PD-L1, HLA-ABC e HLA-DR; produção de IL-10 e TGF-beta1, por ELISA; e ainda em ensaio funcional, que se deu pela co-cultura das DCs com linfócitos T (CD3+, CD3+CD25neg ou CD4+CD25neg), isolados por microsferas imunomagnéticas. Após co-cultura, a expressão de CD25, a proliferação (diluição de CFSE), a produção de citocinas (IFN-g, IL-10, TGF-beta1) e a geração de células Tregs foram analisadas. As células foram caracterizadas como Tregs por seu fenótipo (CD4+CD25+CD127lowCTLA-4+Foxp3+) e sua capacidade supressora sobre linfócitos alogeneicos. iDCs de pacientes apresentaram aumento da expressão de CD86 (com duas subpopulações: CD86High e CD86Low) e CD123 além de produção elevada de IL-10 e TGF-beta1 bioativo. Co-culturas com DCs de pacientes apresentaram níveis altos de TGF-beta1 bioativo (298,08 pg/ml x ctrl: 57,63 pg/ml) e induziram um alta freqüência de Tregs (iDCs: 57% ± 4,1; mDCs: 48% ± 5,0 x ctrl: 2,5% ± 0,7) a partir de precursores CD25negFoxp3neg, que foram capazes de suprimir a proliferação de linfócitos alogeneicos. O bloqueio de TGF-beta nas co-culturas reduziu parcialmente a freqüência de Treg geradas por DCs de pacientes. Esses achados são condizentes com a alta freqüência de Tregs no sangue periférico dessas mesmas pacientes (19,5% ± 2,3 x 8% ± 2,3) e com a presença de células com fenótipo de DCs no sangue, apresentando marcação semelhante a iDCs geradas in vitro. Por outro lado, iDCs provenientes de doadoras saudáveis induziram estimulação linfocitária mais intensa (35,7% ± 7,9 x 11,8 ± 5,9% CD25+), intensa proliferação de linfócitos CD4+ (82,7% x 29,4%) e CD8+ (73,8% x 21%) e alta produção de IFN-g (109,85 pg/ml x 7,86 pg/ml) nas co-culturas. Estes dados indicam que DCs derivadas de monócitos de pacientes com câncer de mama apresentam um viés imunossupressor que não é estritamente dependente do seu status de maturação ou de TGF-beta. Esses achados além de contribuir para a compreensão das interações entre o sistema imune e as neoplasias, devem ser considerados no delineamento de protocolos imunoterapêuticos baseados em DCs.
Dendritic cells (DCs) are the most effective professional antigen-presenting cells. Even considering the possibility of generating DCs in vitro, which allowed the design of antitumor vaccination protocols, mechanisms of peripheral tolerance mediated by regulatory T cells prevent an effective antitumor immune response. The aim of our study was evaluate, in vitro, the induction of regulatory T cells by dendritic cells derived from breast cancer patients.DCs were differentiated from breast cancer patients blood monocytes, for seven days, in the presence of GM-CSF and IL-4 (immature DCs- iDCs) and activated by TNF-a on day five of culture (mature DCs- mDCs). DCs were characterized by flow cytometry to CD1a, CD11c, CD14, CD80, CD86, CD83, CD123, PD-L1, HLA-ABC and HLA-DR expression; the cytokine secretion to IL-10 and bioactive TGF-beta1, by ELISA; and in functional assay by co-culturing DCs with T lymphocytes (CD3+, CD3+CD25neg or CD4+CD25neg) isolated by microbeads. Cell activation (CD25 expression), proliferation (CFSE dilution), cytokine production (IFN-gamma, IL-10 and TGF-beta1) and de novo regulatory T cells (Tregs) generation, were analyzed in these co-cultures after 5 or 6 days. Tregs were characterized by their phenotype (CD4+CD25+CD127LowCTLA-4+Foxp3+) and suppressive capability on allogeneic T cell proliferation. Patients iDCs showed a higher expression of CD86 (two subpopulation: CD86High and CD86Low) and CD123 beyond the elevated production of IL-10 and bioactive TGF-beta1. Co-cultures using patients DCs presented high levels of bioactive TGF-beta1 (298.08 pg/ml x ctrl: 57.63 pg/ml) and induced elevated frequency of Tregs (iDCs: 57% ± 4.1; mDCs: 48% ± 5.0 x ctrl: 2.5% ± 0.7) from CD25neg Foxp3neg precursors, which were able to suppress the allogeneic lymphocyte proliferation. The TGF-beta blocking partially reduced the frequency of induced Tregs by patients DCs. These findings are consistent with the higher frequency of Tregs on peripheral blood of those patients (19.5% ± 2.3 x ctrl 8% ± 2.3) and the presence of DCs also on the blood, showing similar markings with iDCs generated in vitro. Contrastingly, iDCs from healthy donors were better stimulator cells, leading to a higher CD25+ cell frequency (ctrl 35.7% ± 7.9 x 11.8 ± 5.9% CD25+), more intense proliferation of CD4+ (82.7% x 29.4%) and CD8+ (73.8% x 21%) cells and higher production of IFN-gamma (109.85 pg/ml x 7.86 pg/ml) on co-cultures. These data indicate that DCs derived from breast cancer patients show an immunosuppressive bias that is not strictly dependent on DCs maturation status or TGF-beta. Finally, these observations call to caution in the use of patients monocytes for the generation of DC-based vaccines and also contribute to the comprehension of the interactions between the immune system and cancer.

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Horne, Phillip Howard. "Activation and effector function of unconventional acute rejection pathways studied in a hepatocellular allograft model." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1188397900.

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Brandmaier, Andrew G. "TRP-1 AS A MODEL TUMOR ANTIGEN FOR IMMUNOTHERAPY AND IMMUNE TOLERANCE IN THE THYMUS." Thesis, 2011. http://hdl.handle.net/1805/2639.

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Indiana University-Purdue University Indianapolis (IUPUI)
Tolerance mechanisms, which collectively work to prevent autoimmunity, play a key role in suppressing the adaptive immune response to tumor antigens. This phenomenon is attributed to the extensive overlap of tumor associated antigens with self peptides. We studied immune tolerance to tumor antigen TRP-1, a melanoma associated glycoprotein. Vaccination of Wild type (WT) and TRP-1 deficient (Bw) mice with TRP-1 antigen highlighted the substantial effect of tolerance on the T cell response: in the Bw population a log-fold differential was observed with greater clonal numbers and higher intensity of cytokine release from the antigen specific CD4+ T cell population. Additionally, TRP-1-reactive T cells derived from Bw mice demonstrated significantly more efficacious tumor treatment ability than WT donor cells when adoptively transferred into recipients challenged with B16 melanoma. Furthermore, donor Bw T cells were so potent as to overcome suppression by endogenous Tregs in mediating their effect. Probing for a tolerance mechanism, we isolated medullary thymic epithelial cells (mTECs) from WT mice and found that they promiscuously express TRP-1. Unexpectedly, TRP-1 expression in mTECs was found to occur independently of the prominent Autoimmune Regulator (Aire) transcription factor as well as the melanocyte specific transcription factor, mMitf. Our most recent data suggests that thymic dendritic cells may also express copies of the TRP-1 transcript. Future transplant studies will test whether mTECs or thymic dendritic cells directly tolerize TRP-1 specific T cells. Overall, these findings highlight the relevance of central tolerance to cancer immunology and compel further investigation of its mechanistic impact on the development of tumor-reactive T cells.bb

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Books on the topic "T cells. Suppressor cells. Immunological tolerance"

1

A, Berzofsky Jay, and SpringerLink (Online service), eds. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. New York, NY: Springer Science+Business Media, LLC, 2012.

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J, Fairchild Paul, ed. Immunological tolerance: Methods and protocols. Totowa, N.J: Humana Press, 2007.

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3

David, Naor, ed. Immunosuppression and human malignancy. Clifton, N.J: Humana Press, 1989.

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Berzofsky, Jay A., and Masaki Terabe. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. Humana, 2013.

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Berzofsky, Jay A., and Masaki Terabe. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. Springer, 2011.

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6

W, Alt Frederick, and Vogel Henry J. 1920-, eds. Molecular mechanisms of immunological self-recognition. San Diego: Academic Press, 1993.

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D, Kendall Marion, and Ritter Mary A, eds. The Role of the thymus in tolerance induction. Chur: Harwood Academic Publishers, 1990.

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Bishop, Dennis Keith. Influence of in vitro stimulation on T lymphocyte subset involvement in adoptive anti-Listeria immunity. 1986.

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Book chapters on the topic "T cells. Suppressor cells. Immunological tolerance"

1

Pooter, Renée F., and Juan Carlos Zúñiga-Pflücker. "Generation of Immunocompetent T Cells from Embryonic Stem Cells." In Immunological Tolerance, 73–81. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-395-0_5.

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Gregori, Silvia, Rosa Bacchetta, Laura Passerini, Megan K. Levings, and Maria Grazia Roncarolo. "Isolation, Expansion, and Characterization of Human Natural and Adaptive Regulatory T Cells." In Immunological Tolerance, 83–105. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-395-0_6.

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Serafini, Paolo, and Vincenzo Bronte. "Myeloid-Derived Suppressor Cells in Tumor-Induced T Cell Suppression and Tolerance." In Tumor-Induced Immune Suppression, 99–150. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_4.

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Roux, M. E., and M. C. López. "Oral tolerance mediated by dextrin-specific suppressor T cells, migrating from Peyer’s patches to spleen." In Advances in Mucosal Immunology, 274–75. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_77.

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Basten, A., J. Gibson, R. H. Loblay, K. L. Wong, and B. Fazekas de St Groth. "The Role of Memory Suppressor T Cells in Self Tolerance: Induction in Utero and in Athymic Mice." In Microenvironments in the Lymphoid System, 511–20. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2463-8_63.

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Sakaguchi, Shimon, Shohei Hori, Yoshinori Fukui, Takehiko Sasazuki, Noriko Sakaguchi, and Takeshi Takahashi. "Thymic Generation and Selection of CD25+ CD4+ Regulatory T Cells: Implications of Their Broad Repertoire and High Self-Reactivity for the Maintenance of Immunological Self-Tolerance." In Novartis Foundation Symposia, 6–23. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470871628.ch2.

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Goldfarb, Yael, Cristina Peligero-Cruz, and Jakub Abramson. "Immunological Tolerance—T Cells." In The Autoimmune Diseases, 65–90. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-812102-3.00005-1.

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Hamilton, Sara R., Sarah Q. Crome, and Pamela S. Ohashi. "Immunological Tolerance—T Cells." In The Autoimmune Diseases, 87–102. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-384929-8.00007-1.

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JANEWAY, CHARLES A., and YANG LIU. "Activation-Induced Cell Death of Effector T Cells: A Third Mechanism of Immune Tolerance." In Molecular Mechanisms of Immunological Self-Recognition, 159–64. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-053750-1.50018-0.

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Conference papers on the topic "T cells. Suppressor cells. Immunological tolerance"

1

Meng, Wilson S., Jeffrey R. Kovacs, and Ellen S. Gawalt. "The Use of Non-Viral Nucleic Acids Carriers for the Modulation of Leukocytes." In ASME 2008 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2008. http://dx.doi.org/10.1115/smasis2008-348.

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Abstract:

Induction of drug-free permanent organ accommodation is the ultimate goal of transplant therapy. Current pharmacological agents, however, are non-specific in their actions and generally do not confer immunological tolerance. Inhibitors of T cell receptor signaling (tacrolimus and cyclosporine A) represent the mainstay in transplant management. These agents exert their therapeutic effects by dampening the activities of all T cells. Chronic exposure to these agents increases the risk of developing opportunistic infections and malignancies. Given that more than 20,000 Americans undergo organ transplantations each year, there is an urgent need to develop specific therapies to mitigate graft rejection and create conditions conducive for long-term transplant accommodation.

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Koller, U., I. Pabinger, K. Lechner, and W. Knapp. "HEAT INACTIVATED HIGHLY PURIFIED FACTOR VIII CONCENTRATE IN THE TREATMENT OF HEMOPHILIACS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644057.

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51 severe hemophiliacs who had previously been treated with not virus-inactivated intermediate purity factor VIII concentrates were divided into two groups according to their immunological status. Group A (n=23) consisted of patients with CD4/CD8 (helper/suppressor) T cell ratio of 1.0, group B (n=28) of . patients with a ratio of 1.0. In patients of group A treatment was switched in May 1983 to highly purified heat inactivated factor VIII concentrate (BEHRINGWERKE GmbH, Marburg) whereas patients of group B continued to receive intermediate purity factor VIII concentrate. In both groups laboratory tests (clinical investigation, routine liver function tests, differential blood count, lymphocyte subpopulations and quantitative immunoglobulin analysis) were performed in May 1983 and repeated 6, 12 and 18 months thereafter. In group A a significant reduction (p 0.005) of CD8 positive cells from 10587/μl (median) to 540/μl (18 months) was observed; no significant changes of CD8 positive cells occurred in group B. CD4/CD8 ratio rose from 0.58 to 0.86 in group A (p = 0.005) and remained unchanged in group B (1.38 versus 1.23). Serum IgG decreased in both groups but was more pronounced in group A. Thus treatment with heat inactivated highly purified factor VIII improved the immunological status of hemophiliacs with an inverse ratio. Retrospective analysis of antibodies to HIV, however, showed that most of the patients of group A were antibody positive (n=21), but the 2 negative patients remained negative. In group B of the 10 HIV negative patients one became positive, all others did not change. Whether this improvement of immunological laboratory findings is of clinical relevance, remains to be established, particularly with respect to the high incidence of antibody positive patients within group A.

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