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Literature DB >> 19234160

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

Ines Gonzalez-García¹, Yani Zhao, Songguang Ju, Qin Gu, Lin Liu, Jay K Kolls, Binfeng Lu.

Abstract

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.

Entities: Chemical Disease Gene Species

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Year: 2009 PMID： 19234160 PMCID： PMC2800821 DOI： 10.4049/jimmunol.0802221

Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422

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