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Cytokines in the induction and resolution of experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis is the prototypic T cell-mediated autoimmune disease model. Classically, this disease was viewed in terms of type 1 versus type 2 immunity: the type 1 cytokines IFNγ and TNFα promoting disease, whereas an IL-4-dominated, type 2 response was protective. Howev...

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Bibliographic Details
Published in:Cytokine (Philadelphia, Pa.) Pa.), 2005-10, Vol.32 (2), p.81-84
Main Authors: McGeachy, Mandy J., Anderton, Stephen M.
Format: Article
Language:English
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Summary:Experimental autoimmune encephalomyelitis is the prototypic T cell-mediated autoimmune disease model. Classically, this disease was viewed in terms of type 1 versus type 2 immunity: the type 1 cytokines IFNγ and TNFα promoting disease, whereas an IL-4-dominated, type 2 response was protective. However, studies in knockout mice do not support this paradigm. More recent data point to important roles for IL-23 and IL-17 (rather than IL-12 and IFNγ) in the establishment and persistence of the inflammatory lesion. IL-10 appears to be the dominant cytokine mediating recovery. The source of IL-10 includes B cells (most probably in the peripheral lymphoid organs). However, the key IL-10-producing cell within the central nervous system is a CD4 +CD25 + T cell population that has regulatory function and is critical to resolution of the disease.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2005.07.012