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: 31 July 2025

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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 (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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2

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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3

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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4

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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5

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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7

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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10

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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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 cont
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