IL-17 signaling-independent central nervous system autoimmunity is negatively regulated by TGF-β
I Gonzalez-García, Y Zhao, S Ju, Q Gu… - The Journal of …, 2009 - journals.aai.org
The Journal of Immunology, 2009•journals.aai.org
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-β 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 …
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-β 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 …
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-β 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-β.
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