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Publication : IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta.

First Author  Gonzalez-García I Year  2009
Journal  J Immunol Volume  182
Issue  5 Pages  2665-71
PubMed ID  19234160 Mgi Jnum  J:146264
Mgi Id  MGI:3837102 Doi  10.4049/jimmunol.0802221
Citation  Gonzalez-Garcia I, et al. (2009) IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta. J Immunol 182(5):2665-71
abstractText  Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA)(-/-) mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-beta in IL-17RA(-/-) mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA(-/-) mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-beta.
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