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Bibliographies thématiques / Experimental autoimmune encephalomyelitis, mast cells, histamine / Articles de revues

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Articles de revues sur le sujet « Experimental autoimmune encephalomyelitis, mast cells, histamine »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Dietsch, G. N., and D. J. Hinrichs. "The role of mast cells in the elicitation of experimental allergic encephalomyelitis." Journal of Immunology 142, no. 5 (1989): 1476–81. http://dx.doi.org/10.4049/jimmunol.142.5.1476.

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Abstract Experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease can be transferred with lymphoid cells from actively immunized rats into naive recipients. In the mouse, previous studies have suggested a role for histamine/serotonin in the development of active EAE. We have found that myelin basic protein-reactive cells transfer a biphasic skin test response to naive rats analogous to what has been described in the mouse contact dermatitis system, where mast cell sensitization by Ag-specific T cell factors is required for the induction of skin test responses. Treatm

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Musio, Silvia, Massimo Costanza, Pietro Luigi Poliani та ін. "Treatment with anti-FcεRIα antibody exacerbates EAE and T-cell immunity against myelin". Neurology - Neuroimmunology Neuroinflammation 4, № 3 (2017): e342. http://dx.doi.org/10.1212/nxi.0000000000000342.

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Objective:To investigate the effects of targeting the high-affinity receptor for immunoglobulin E (FcεRI), that plays a central role in allergic responses and is constitutively expressed on mast cells and basophils, in clinical disease and autoimmune T-cell response in experimental MS.Methods:Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein 35–55. Anti-FcεRI α-chain antibody was administered intraperitoneally. CNS immunohistochemistry, flow cytometry analysis of immune cell populations, IgE and histamine serum

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Costanza, Massimo, Mario Colombo, and Rosetta Pedotti. "Mast Cells in the Pathogenesis of Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." International Journal of Molecular Sciences 13, no. 12 (2012): 15107–25. http://dx.doi.org/10.3390/ijms131115107.

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Yin, Jun-Jie, Xue-Qiang Hu, Zhi-Feng Mao, et al. "Neutralization of Interleukin-9 Decreasing Mast Cells Infiltration in Experimental Autoimmune Encephalomyelitis." Chinese Medical Journal 130, no. 8 (2017): 964–71. http://dx.doi.org/10.4103/0366-6999.204110.

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Elieh-Ali-Komi, Daniel, and Yonghao Cao. "Role of Mast Cells in the Pathogenesis of Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis." Clinical Reviews in Allergy & Immunology 52, no. 3 (2016): 436–45. http://dx.doi.org/10.1007/s12016-016-8595-y.

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Russi, Abigail E., Mark E. Ebel, Yuchen Yang, and Melissa A. Brown. "Male-specific IL-33 expression regulates sex-dimorphic EAE susceptibility." Proceedings of the National Academy of Sciences 115, no. 7 (2018): E1520—E1529. http://dx.doi.org/10.1073/pnas.1710401115.

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The cellular and molecular basis of sex-dimorphic autoimmune diseases, such as the CNS demyelinating disease multiple sclerosis (MS), remains unclear. Our studies in the SJL mouse model of MS, experimental autoimmune encephalomyelitis (EAE), reveal that sex-determined differences in Il33 expression by innate immune cells in response to myelin peptide immunization regulate EAE susceptibility. IL-33 is selectively induced in PLP139–151-immunized males and activates type 2 innate lymphoid cells (ILC2s), cells that promote and sustain a nonpathogenic Th2 myelin-specific response. Without this atte

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Hatfield, Julianne, and Melissa Brown. "The meninges: A staging site for immune cell interactions in early experimental autoimmune encephalomyelitis (P4166)." Journal of Immunology 190, no. 1_Supplement (2013): 172.10. http://dx.doi.org/10.4049/jimmunol.190.supp.172.10.

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Abstract Multiple sclerosis (MS) is a demyelinating disease affecting the central nervous system in which immune mediate damage to white matter myelin is well characterized. However, improved imaging has revealed that inflammation in the meninges, tissues that are proximal to the CNS, also occurs and corresponds to cortical grey matter lesion formation in early disease. Together with evidence of activated T cells and tertiary lymphoid follicle formation within these tissues, these data suggest that the meninges are critical sites of immune cell activity. Yet little is known about the basal and

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Teuscher, Cory, Meena Subramanian, Rajkumar Noubade, et al. "Central Histamine H3 Receptor Signaling Negatively Regulates Autoimmune Inflammation (129.31)." Journal of Immunology 178, no. 1_Supplement (2007): S223. http://dx.doi.org/10.4049/jimmunol.178.supp.129.31.

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Abstract Histamine is a ubiquitous regulator of diverse physiologic processes including inflammation, immune modulation and neurotransmission. Four subtypes of histamine receptors are currently recognized and genetic and pharmacological studies have shown that the H1 and H2 receptors play a role in susceptibility to experimental allergic encephalomyelitis (EAE), the primary autoimmune model of multiple sclerosis. Histamine H3 receptor (H3R), which is not expressed in hematopoietic cells, is a presynaptic auto- and hetero-receptor. Here we show that H3RKO mice develop significantly more severe

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Secor, Virginia H., W. Evan Secor, Claire-Anne Gutekunst, and Melissa A. Brown. "Mast Cells Are Essential for Early Onset and Severe Disease in a Murine Model of Multiple Sclerosis." Journal of Experimental Medicine 191, no. 5 (2000): 813–22. http://dx.doi.org/10.1084/jem.191.5.813.

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In addition to their well characterized role in allergic inflammation, recent data confirm that mast cells play a more extensive role in a variety of immune responses. However, their contribution to autoimmune and neurologic disease processes has not been investigated. Experimental allergic encephalomyelitis (EAE) and its human disease counterpart, multiple sclerosis, are considered to be CD4+ T cell–mediated autoimmune diseases affecting the central nervous system. Several lines of indirect evidence suggest that mast cells could also play a role in the pathogenesis of both the human and murin

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ORR, EDWARD L. "Presence and Distribution of Nervous System-Associated Mast Cells That May Modulate Experimental Autoimmune Encephalomyelitis." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (1988): 723–26. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27226.x.

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Orr, Edward L. "Presence and distribution of nervous system — associated mast cells which may modulate experimental autoimmune encephalomyelitis." Journal of Neuroimmunology 16, no. 1 (1987): 136. http://dx.doi.org/10.1016/0165-5728(87)90341-9.

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Bicer, Fuat, Cengiz Z. Altuntas, Kenan Izgi, et al. "Chronic pelvic allodynia is mediated by CCL2 through mast cells in an experimental autoimmune cystitis model." American Journal of Physiology-Renal Physiology 308, no. 2 (2015): F103—F113. http://dx.doi.org/10.1152/ajprenal.00202.2014.

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The cause of chronic pelvic pain in interstitial cystitis/painful bladder syndrome (IC/PBS) remains unclear; autoimmunity is a possible etiology. We have recently shown that injection of a single immunogenic peptide of uroplakin 3A (UPK3A 65-84) induces experimental autoimmune cystitis (EAC) in female BALB/cJ mice that is unique among experimental models in accurately reflecting both the urinary symptoms and pelvic pain of IC/PBS. The aim of this project was to identify the roles of mast cells and mast cell chemoattractant/activator monocyte chemoattractant protein-1 [chemokine (C-C motif) lig

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Desbiens, Louisane, Catherine Lapointe, Marjan Gharagozloo, et al. "Significant Contribution of Mouse Mast Cell Protease 4 in Early Phases of Experimental Autoimmune Encephalomyelitis." Mediators of Inflammation 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/9797021.

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Experimental autoimmune encephalomyelitis (EAE) is a mouse model that reproduces cardinal signs of clinical, histopathological, and immunological features found in Multiple Sclerosis (MS). Mast cells are suggested to be involved in the main inflammatory phases occurring during EAE development, possibly by secreting several autacoids and proteases. Among the latter, the chymase mouse mast cell protease 4 (mMCP-4) can contribute to the inflammatory response by producing endothelin-1 (ET-1). The aim of this study was to determine the impact of mMCP-4 on acute inflammatory stages in EAE. C57BL/6 w

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Weiskirchen, Ralf, Steffen K. Meurer, Christian Liedtke, and Michael Huber. "Mast Cells in Liver Fibrogenesis." Cells 8, no. 11 (2019): 1429. http://dx.doi.org/10.3390/cells8111429.

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Mast cells (MCs) are immune cells of the myeloid lineage that are present in the connective tissue throughout the body and in mucosa tissue. They originate from hematopoietic stem cells in the bone marrow and circulate as MC progenitors in the blood. After migration to various tissues, they differentiate into their mature form, which is characterized by a phenotype containing large granules enriched in a variety of bioactive compounds, including histamine and heparin. These cells can be activated in a receptor-dependent and -independent manner. Particularly, the activation of the high-affinity

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Brown, Melissa Ann, and Yuchen Yang. "Distinct chromatin modifications at the Il33 locus in mast cells contribute to sex dimorphic susceptibility to EAE, an autoimmune CNS demyelinating disease." Journal of Immunology 204, no. 1_Supplement (2020): 219.8. http://dx.doi.org/10.4049/jimmunol.204.supp.219.8.

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Abstract Many autoimmune diseases, including multiple sclerosis (MS) exhibit a striking female bias, but the underlying mechanisms remain poorly understood. Using the SJL mouse model of MS, experimental autoimmune encephalomyelitis (EAE), which recapitulates this sex dimorphism, we previously demonstrated that preferential IL-33 expression contributes to male protection. IL-33 expression by mast cells in PLP139–151-immunized males activates type 2 innate lymphoid cells, which in turn drives a non-pathogenic Th2 response to myelin peptide. Testosterone directly activates Il33 in male but not fe

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Saligrama, Naresha, Rajkumar Noubade, Laure Case, Matthew Poynter, and Cory Teuscher. "H1R signaling in antigen presenting cells is dispensable for eliciting pathogenic T cells in experimental allergic encephalomyelitis (123.14)." Journal of Immunology 188, no. 1_Supplement (2012): 123.14. http://dx.doi.org/10.4049/jimmunol.188.supp.123.14.

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Abstract The histamine H1 receptor (Hrh1/H1R) was identified as a shared autoimmune disease (SAID) gene in experimental allergic encephalomyelitis (EAE) and autoimmune orchitis, the principal AI models of multiple sclerosis (MS) and idiopathic male infertility, respectively. As a SAID gene, Hrh1/H1R can exert effects in multiple cell types including endothelial cells, T cells, and antigen presenting cells at critical check points during both the induction and effector phases of disease. In this regard, we showed that selective re-expression of H1R by endothelial cells in Hrh1-KO (H1RKO) mice s

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Aldossari, Abdullah A., Mohammed A. Assiri, Mushtaq A. Ansari, et al. "Histamine H4 Receptor Antagonist Ameliorates the Progression of Experimental Autoimmune Encephalomyelitis via Regulation of T-Cell Imbalance." International Journal of Molecular Sciences 24, no. 20 (2023): 15273. http://dx.doi.org/10.3390/ijms242015273.

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Multiple sclerosis (MS) is a degenerative condition characterized by immune-mediated attacks on the central nervous system (CNS), resulting in demyelination and recurring T-cell responses. The histamine H4 receptor (H4R) is mainly expressed in cellular populations and plays a vital role in inflammation and immunological responses. The role of H4R in neurons of the CNS has recently been revealed. However, the precise role of H4R in neuronal function remains inadequately understood. The objective of this work was to investigate the impact of JNJ 10191584 (JNJ), a highly effective and specific H4

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Finlay, Conor M., Kyle T. Cunningham, Benjamin Doyle, and Kingston H. G. Mills. "IL-33–Stimulated Murine Mast Cells Polarize Alternatively Activated Macrophages, Which Suppress T Cells That Mediate Experimental Autoimmune Encephalomyelitis." Journal of Immunology 205, no. 7 (2020): 1909–19. http://dx.doi.org/10.4049/jimmunol.1901321.

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Shi, Yaru, Zhenlong Li, Ran Chen, et al. "Immethridine, histamine H3-receptor (H3R) agonist, alleviated experimental autoimmune encephalomyelitis via inhibiting the function of dendritic cells." Oncotarget 8, no. 43 (2017): 75038–49. http://dx.doi.org/10.18632/oncotarget.20500.

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Brown, Melissa Ann, and Yuchen Yang. "Distinct chromatin modifications at the Il33 locus in mast cells contribute to sex dimorphic susceptibility to EAE, an autoimmune CNS demyelinating disease." Journal of Immunology 206, no. 1_Supplement (2021): 64.15. http://dx.doi.org/10.4049/jimmunol.206.supp.64.15.

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Abstract Many autoimmune diseases, including multiple sclerosis (MS), exhibit a striking female bias, but the underlying mechanisms remain poorly understood. Using the SJL mouse model of MS, experimental autoimmune encephalomyelitis (EAE), which recapitulates this sex dimorphism, we previously demonstrated that preferential IL-33 expression contributes to male protection. IL-33 expression by mast cells in PLP139–151-immunized males activates type 2 innate lymphoid cells, which in turn drives a non-pathogenic Th2 response to myelin peptide. Testosterone directly activates Il33 in male but not f

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Nowak, Elizabeth C., Casey T. Weaver, Henrietta Turner, et al. "IL-9 as a mediator of Th17-driven inflammatory disease." Journal of Experimental Medicine 206, no. 8 (2009): 1653–60. http://dx.doi.org/10.1084/jem.20090246.

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We report that like other T cells cultured in the presence of transforming growth factor (TGF) β, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-β as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with

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Hong, Gwan Ui, Young Min Ahn, and Jai Youl Ro. "Transglutaminase 2 over-Expressed By Interaction of Mast Cells and Oligodendrocytes Induces Demyelination in the Experimental Autoimmune Encephalomyelitis." Journal of Allergy and Clinical Immunology 137, no. 2 (2016): AB76. http://dx.doi.org/10.1016/j.jaci.2015.12.257.

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Piconese, Silvia, Giorgia Gri, Claudio Tripodo, et al. "Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation." Blood 114, no. 13 (2009): 2639–48. http://dx.doi.org/10.1182/blood-2009-05-220004.

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Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of

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Noubade, Rajkumar, Mercedes Rincon, and Cory Teuscher. "IFN-gamma production by CD4 T cells requires Histamine H1 receptor during their initial phase of activation (87.25)." Journal of Immunology 178, no. 1_Supplement (2007): S132. http://dx.doi.org/10.4049/jimmunol.178.supp.87.25.

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Abstract Histamine H1 receptor (H1R) signaling in T cells plays an important role Th1 effector functions. H1R is an autoimmune susceptibility gene controlling experimental autoimmune encephalomyelitis (EAE). H1R knockout (H1RKO) mice also develop significantly less severe EAE compared to C57BL/6J wild-type mice in association with immune deviation of the CD4+ T-cell response from a Th1- to a Th2-like response. Little is known about the role of direct H1R signaling in the regulation of T-cell effector responses. In this study, T-cells from C57BL/6J and H1RKO mice were used to study H1R signalin

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Piacente, Francesco, Marta Bottero, Andrea Benzi, et al. "Neuroprotective Potential of Dendritic Cells and Sirtuins in Multiple Sclerosis." International Journal of Molecular Sciences 23, no. 8 (2022): 4352. http://dx.doi.org/10.3390/ijms23084352.

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Myeloid cells, including parenchymal microglia, perivascular and meningeal macrophages, and dendritic cells (DCs), are present in the central nervous system (CNS) and establish an intricate relationship with other cells, playing a crucial role both in health and in neurological diseases. In this context, DCs are critical to orchestrating the immune response linking the innate and adaptive immune systems. Under steady-state conditions, DCs patrol the CNS, sampling their local environment and acting as sentinels. During neuroinflammation, the resulting activation of DCs is a critical step that d

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Lee, Sung Won, Hyun Jung Park, Jungmin Jeon, et al. "Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses." International Journal of Molecular Sciences 22, no. 4 (2021): 1553. http://dx.doi.org/10.3390/ijms22041553.

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The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic

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Bennett, Jami L., Marie-Renée Blanchet, Linlin Zhao, et al. "Bone Marrow-Derived Mast Cells Accumulate in the Central Nervous System During Inflammation but Are Dispensable for Experimental Autoimmune Encephalomyelitis Pathogenesis." Journal of Immunology 182, no. 9 (2009): 5507–14. http://dx.doi.org/10.4049/jimmunol.0801485.

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Nowak, Elizabeth C., Victor C. de Vries, Anna Wasiuk, et al. "Tryptophan hydroxylase-1 regulates immune tolerance and inflammation." Journal of Experimental Medicine 209, no. 11 (2012): 2127–35. http://dx.doi.org/10.1084/jem.20120408.

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Nutrient deprivation based on the loss of essential amino acids by catabolic enzymes in the microenvironment is a critical means to control inflammatory responses and immune tolerance. Here we report the novel finding that Tph-1 (tryptophan hydroxylase-1), a synthase which catalyses the conversion of tryptophan to serotonin and exhausts tryptophan, is a potent regulator of immunity. In models of skin allograft tolerance, tumor growth, and experimental autoimmune encephalomyelitis, Tph-1 deficiency breaks allograft tolerance, induces tumor remission, and intensifies neuroinflammation, respectiv

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Hong, Gwan Ui, Nam Goo Kim, Dooil Jeoung, and Jai Youl Ro. "Anti-CD40 Ab- or 8-oxo-dG-enhanced Treg cells reduce development of experimental autoimmune encephalomyelitis via down-regulating migration and activation of mast cells." Journal of Neuroimmunology 260, no. 1-2 (2013): 60–73. http://dx.doi.org/10.1016/j.jneuroim.2013.04.002.

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Alsaad, Abdulaziz M. S., Mushtaq A. Ansari, Ahmed Nadeem, et al. "Histamine H4 Receptor Agonist, 4-Methylhistamine, Aggravates Disease Progression and Promotes Pro-Inflammatory Signaling in B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model." International Journal of Molecular Sciences 24, no. 16 (2023): 12991. http://dx.doi.org/10.3390/ijms241612991.

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We sought to assess the impact of 4-Methylhistamine (4-MeH), a specific agonist targeting the Histamine H4 Receptor (H4R), on the progression of experimental autoimmune encephalomyelitis (EAE) and gain insight into the underlying mechanism. EAE is a chronic autoimmune, inflammatory, and neurodegenerative disease of the central nervous system (CNS) characterized by demyelination, axonal damage, and neurodegeneration. Over the past decade, pharmacological research into the H4R has gained significance in immune and inflammatory disorders. For this study, Swiss Jim Lambert EAE mice were treated wi

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Short, Abigail, Margaret Walker-Caulfield, and Melissa Brown. "c-kit signaling pathways regulate EAE susceptibility in male SJL mice (P3119)." Journal of Immunology 190, no. 1_Supplement (2013): 43.21. http://dx.doi.org/10.4049/jimmunol.190.supp.43.21.

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Abstract Females are more susceptible to autoimmune diseases, including multiple sclerosis (MS), a demyelinating disease of the central nervous system. While genetic, hormonal, and immune differences have been implicated, the mechanism for this female bias remains unclear. The animal model of MS, experimental autoimmune encephalomyelitis (EAE), recapitulates many of the features of the human disease; including the significant sex dimorphism. We previously reported that wild type (WT) female SJL mice exhibit more severe disease than their c-kit mutant counterparts and that this phenotype is mas

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Alrashdi, Barakat, Bassel Dawod, Sabine Tacke, Stefanie Kuerten, Patrice D. Côté, and Jean S. Marshall. "Mice Heterozygous for the Sodium Channel Scn8a (Nav1.6) Have Reduced Inflammatory Responses During EAE and Following LPS Challenge." Frontiers in Immunology 12 (March 19, 2021). http://dx.doi.org/10.3389/fimmu.2021.533423.

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Voltage gated sodium (Nav) channels contribute to axonal damage following demyelination in experimental autoimmune encephalomyelitis (EAE), a rodent model of multiple sclerosis (MS). The Nav1.6 isoform has been implicated as a primary contributor in this process. However, the role of Nav1.6 in immune processes, critical to the pathology of both MS and EAE, has not been extensively studied. EAE was induced with myelin oligodendrocyte (MOG35-55) peptide in Scn8admu/+ mice, which have reduced Nav1.6 levels. Scn8admu/+ mice demonstrated improved motor capacity during the recovery and early chronic

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