IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta.
IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-beta.
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DOI:
10.4049/jimmunol.0802221
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发表时间:
2009-03-01
期刊:
影响因子:
--
通讯作者:
Lu B
中科院分区:
文献类型:
--
作者:
Gonzalez-García I;Zhao Y;Ju S;Gu Q;Liu L;Kolls JK;Lu B
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 (EAE), a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGFβ in IL-17RA−/− mice resulted in much more severe clinical signs of EAE and significantly increased parenchymal lymphocyte infiltration in the central nervous system (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 TGFβ.
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