Relevant bibliographies by topics / Experimental autoimmune encephalomyelitis, mast cells, histamine

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Experimental autoimmune encephalomyelitis, mast cells, histamine'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Experimental autoimmune encephalomyelitis, mast cells, histamine"

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 (March 1, 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. Treatment of cell recipients with the serotonin receptor antagonists, cyproheptadine or methysergide, blocked or significantly reduced the development of EAE. Furthermore, it was found that treatment with cyproheptadine was effective in blocking clinical disease when administered day 3 to day 6 after cell transfer. In contrast, cyproheptadine treatments before induction of paralysis day 0 to 3, failed to alter the course of clinical disease. The inhibitor of mast cell degranulation, proxicromil, was also found to effectively block the elicitation of adoptively transferred EAE and was also found to be effective when administered just before the onset of clinical disease. Reserpine, a compound known to deplete mast cells of vasoactive amines by forcing granule contents into the cytoplasm where they are degraded by cell enzymes, was also effective in blocking both active and adoptively transferred EAE. Disease inhibition was found to be partially reversed with pargyline, an inhibitor of monoamine oxidase. In addition lymphocytes from treated animals were capable of transferring disease to naive recipients and appeared to have normal activity as assessed by Ag-or mitogen-driven proliferation in addition to IL-2 production.
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Musio, Silvia, Massimo Costanza, Pietro Luigi Poliani, Elena Fontana, Manuela Cominelli, Gabriella Abolafio, Lawrence Steinman, and Rosetta Pedotti. "Treatment with anti-FcεRIα antibody exacerbates EAE and T-cell immunity against myelin." Neurology - Neuroimmunology Neuroinflammation 4, no. 3 (April 14, 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 concentration, immune cell proliferation, and cytokine measurement were performed. In BALB/c mice, EAE was induced by immunization with myelin proteolipid protein 185–206.Results:Treatment with anti-FcεRIα antibody resulted in exacerbation of EAE and increased CNS inflammation in C57BL/6 mice. Treated mice displayed long-lasting complete depletion of basophils in the blood stream and peripheral lymphoid organs and increased antigen-induced immune cell proliferation and production of interferon-γ, interleukin (IL)-17, IL-6, and granulocyte-macrophage colony-stimulating factor. In BALB/c mice, which are T-helper (Th) 2 prone and resistant to EAE, treatment with anti-FcεRIα antibody restored susceptibility to EAE.Conclusion:Our observations that anti-FcεRIα antibody increases Th1 and Th17 responses against myelin antigen and exacerbates EAE suggest that FcεRI, basophils, and possibly other FcεRI-bearing cells that might be affected by this antibody play important roles in influencing the severity of CNS autoimmunity.
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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 (November 16, 2012): 15107–25. http://dx.doi.org/10.3390/ijms131115107.

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Yin, Jun-Jie, Xue-Qiang Hu, Zhi-Feng Mao, Jian Bao, Wei Qiu, Zheng-Qi Lu, Hao-Tian Wu, and Xiao-Nan Zhong. "Neutralization of Interleukin-9 Decreasing Mast Cells Infiltration in Experimental Autoimmune Encephalomyelitis." Chinese Medical Journal 130, no. 8 (April 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 (December 26, 2016): 436–45. http://dx.doi.org/10.1007/s12016-016-8595-y.

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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 (November 1988): 723–26. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27226.x.

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7

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

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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 (May 1, 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 disease-associated immune status of these tissues. Using a murine model of MS, we evaluated the immune cell makeup of the meninges in naïve mice and asked how this changes during the course of disease. CD4+ and CD8+ T cells, macrophages, dendritic cells, mast cells and neutrophils are detected in naïve mice and increased numbers of neutrophils and macrophages are observed in preclinical disease. A population of innate lymphoid cells (ILCs: CD3-, CD4+/-, RORγt+, IL-7Rα+) also normally resides in the meninges and this population is reduced in mast cell deficient mice. These data confirm that the meninges are an active site of immune response in early disease. We speculate that meningeal ILCs may provide a mechanism for the development of tertiary lymphoid follicle formation as well as contribute to Th17 cell activation and thereby amplify meningeal inflammation.
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Teuscher, Cory, Meena Subramanian, Rajkumar Noubade, Jian Feng Gao, Halina Offner, James F. Zachary, and Elizabeth P. Blankenhorn. "Central Histamine H3 Receptor Signaling Negatively Regulates Autoimmune Inflammation (129.31)." Journal of Immunology 178, no. 1_Supplement (April 1, 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 acute phase clinical disease and neuropathology compared to wild-type controls. In H3RKO mice this is preceded by disruption of the blood brain barrier and increased chemokine/chemokine receptor expression in peripheral T-cells. These data are consistent with inhibition of H3R-mediated neurogenic control of cerebrovascular tone and T-cell function. Additionally, genetic studies indicate that an H3R polymorphism leading to differential expression of H3R isoforms underlies eae8, a locus controlling disease associated weight loss, a phenotype known to be regulated by central H3R activity.
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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 (January 29, 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 attenuating IL-33 response, females generate an encephalitogenic Th17-dominant response, which can be reversed by IL-33 treatment. Mast cells are one source of IL-33 and we provide evidence that testosterone directly induces Il33 gene expression and also exerts effects on the potential for Il33 gene expression during mast cell development. Thus, in contrast to their pathogenic role in allergy, we propose a sex-specific role for both mast cells and ILC2s as attenuators of the pathogenic Th response in CNS inflammatory disease.
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Dissertations / Theses on the topic "Experimental autoimmune encephalomyelitis, mast cells, histamine"

1

COSTANZA, MASSIMO. "Mast cells in the pathogenesis of experimental multiple sclerosis." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29633.

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Mast cell (MC)-deficient c-Kit mutant KitW/W-v mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. However studies performed so far on this topic relied on a single model of MC-deficiency, the KitW/W-v, which bears several c-Kit dependent phenotypic abnormalities other than MC-deficiency, such as neutropenia and anaemia. Also, it is not clear how MCs shape the central nervous system (CNS) autoimmune response occurring in EAE. In the first work, we focused on evaluating the contribution of MCs to EAE in both KitW/W-v mice and in a newly characterized MC-deficient strain, KitW-sh/W-sh, which seems to bear fewer c-Kit dependent hematopoietic alterations. We also aimed at characterizing the T cell response to myelin antigen in a context of MC-deficiency. The comprehension of how mast cells intervene in the pathology of EAE and MS might help designing better therapies for these diseases. Histamine is one of the main preformed mediators stored in MC granules. In the second part of the thesis we evaluated the ability of histamine to modulate the response of myelin-activated T cells. We explored the effect of histamine and specific agonists of histamine receptors 1 and 2 on activation and migratory capacity of myelin-autoreactive T cells through the inflamed BBB.
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