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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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Published in: | Cytokine (Philadelphia, Pa.) Pa.), 2005-10, Vol.32 (2), p.81-84 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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. |
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ISSN: | 1043-4666 1096-0023 |
DOI: | 10.1016/j.cyto.2005.07.012 |