Journal
JOURNAL OF IMMUNOLOGY
Volume 182, Issue 5, Pages 2665-2671Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802221
Keywords
-
Categories
Funding
- NIAID NIH HHS [R01 AI063496-04, R01 AI063496, R01 AI063496-02, R01 AI063496-01A1, AI063496, R01 AI063496-03] Funding Source: Medline
- NIAMS NIH HHS [P30 AR047372, K01 AR048854, P30-AR47372, 1 K01 AR048854] Funding Source: Medline
Ask authors/readers for more resources
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 tells 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. The Journal of Immunology, 2009, 182: 2665-2671.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
