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Toll‐like Receptors in Multiple Sclerosis Mouse Experimental Models
Author(s) -
Marta Monica
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04849.x
Subject(s) - experimental autoimmune encephalomyelitis , tlr3 , immunology , immune system , receptor , pattern recognition receptor , biology , proinflammatory cytokine , tlr9 , tlr4 , acquired immune system , toll like receptor , innate immune system , myeloid , inflammation , microbiology and biotechnology , gene expression , gene , biochemistry , dna methylation
Certain pathogen molecules trigger innate immune responses and drive subsequent adaptive immune responses toward an antigen presented simultaneously. Such bacterial or viral molecules constitute pathogen‐associated molecular patterns (PAMPs) that bind to pattern‐recognition receptors such as toll‐like receptors (TLRs). Recently, endogenous molecules were identified that ligate the same receptors. The role of these receptors' response to complete Freund's adjuvant during initiation of CD4 T cell responses in EAE, the animal model for multiple sclerosis, is here discussed. Myeloid differentiation primary response gene 88 (MyD88) is necessary for the induction of experimental autoimmune encephalomyelitis (EAE), and it is required for the activation of myeloid dendritic cells and differentiation of T helper 17 cells. The role of individual TLR, in particular TLR3, TLR4, and TLR9, signaling in modulation of EAE inflammation varies with the experimental model employed and the immune cells that drive pathology. The TLR‐dependent production of proinflammatory cytokines is regulated by mechanisms that dampen the pathway and prevent excess damage. Development of TLR antagonists to treat autoimmune diseases must acknowledge the possibility of interference with regulatory mechanisms.