Hypothesis: a possible role for mast cells and their inflammatory mediators in the pathogenesis of autoimmune encephalomyelitis

• Published in: Journal of neuroscience research Vol. 45; no. 4; pp. 340 - 348
• Main Authors: Bebo Jr, B.F., Yong, T., Orr, E.L., Linthicum, D.S.
• Format: Journal Article
• Language: English
• Published: New York John Wiley & Sons, Inc 15.08.1996
• Subjects: Animals; encephalomyelitis; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - physiopathology; Humans; Inflammation Mediators - immunology; mast cells; Mast Cells - immunology; microcirculation; vasoactive
• ISSN: 0360-4012; 1097-4547
• DOI: 10.1002/(SICI)1097-4547(19960815)45:4<340::AID-JNR3>3.0.CO;2-9

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.