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Hypothesis: a possible role for mast cells and their inflammatory mediators in the pathogenesis of autoimmune encephalomyelitis
Author(s) -
Bebo B.F.,
Yong T.,
Orr E.L.,
Linthicum D.S.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960815)45:4<340::aid-jnr3>3.0.co;2-9
Subject(s) - immunology , experimental autoimmune encephalomyelitis , mast cell , inflammation , histamine , extravasation , multiple sclerosis , central nervous system , tumor necrosis factor alpha , pathogenesis , encephalomyelitis , degranulation , biology , medicine , neuroscience , receptor , biochemistry , endocrinology
Mast cells and their potent chemical mediators are known to initiate and modulate a number of important inflammatory cascades. With respect to the central nervous system, the role of mast cells as participants in the promotion and resolution of inflammation has been widely underestimated. Mast cell‐derived histamine, serotonin, kallikreins, and tumor necrosis factor‐α (TNF‐α) can enhance microvascular permeability, leukocyte rolling, adhesion, and extravasation of inflammatory cells into the brain and spinal cord. Mast cell mediators may play an important role in autoimmune encephalomyelitis and multiple sclerosis by promoting the entry of autoreactive T cells and the recruitment of nonspecific monocytes across the blood:brain barrier. © 1996 Wiley‐Liss, Inc.