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IL‐17 helps autoimmune th1 responses
Author(s) -
gonzalezgarcia ines,
Zhao Yani,
Ju Songguang,
Gu Qin,
Bennett Jennifer,
Liu Lin,
Kolls Jay,
Lu Binfeng
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1073.24
Subject(s) - experimental autoimmune encephalomyelitis , immunology , interleukin 17 , autoimmunity , disease , cytokine , autoimmune disease , medicine , multiple sclerosis , population , immune system , antibody , environmental health
Recent studies have established a critical role of IL‐17 in the initiation of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). In contrast to Th17 cells, the role of Th1 in EAE is controversial, on one hand there is a wealth of evidence supporting the role of Th1 cells in EAE but on the other hand, IFNγ, the hallmark cytokine for Thy1 cells, is not required for the generation of EAE. It is documented that Th17 and Th1 cells co‐exist in autoimmune diseases such as EAE. In addition, CD4 T cells producing both IL‐17 and IFNγ were found and sometimes represented a major population of autoreactive CD4 T cells. Despite these observations, it is not known weather Th17 and Th1 cells affect each other's function during autoimmunity. In this study, it is shown that the interleukin 17A receptor (IL‐17RA) is crucial for the development of EAE. IL‐17RA deficiency results in a delay of disease onset, lessened peak clinical scores, and hastier recoveries. Interestingly, the generation of autoreactive Th1 cells but not Th17 cells is compromised in IL‐17RA −/− mice and disease severity correlated with increased Th1 responses, suggesting EAE amelioration can be attributed to the reduction of Th1 responses. (R01 AI063496 (01/01/2006‐12/31/2010) NIH/NIAID. K01 AR048854 (07/01/2003‐03/31/2008) NIH/NIAMS.)