TY - JOUR
T1 - Aryl hydrocarbon receptor deficiency in T cells suppresses the development of collagen-induced arthritis
AU - Nakahama, Taisuke
AU - Kimura, Akihiro
AU - Trung Nguyen, Nam
AU - Chinen, Ichino
AU - Hanieh, Hamza
AU - Nohara, Keiko
AU - Fujii-Kuriyama, Yoshiaki
AU - Kishimoto, Tadamitsu
PY - 2011/8/23
Y1 - 2011/8/23
N2 - The contributions of aryl hydrocarbon receptor (Ahr) to the pathogenesis of rheumatoid arthritis have not been elucidated. Here, we show that Ahr deficiency ameliorated collagen-induced arthritis, a mouse model of RA. Collagen-immunized Ahr KO mice showed decreased serum levels of such proinflammatory cytokines as IL-1β and IL-6. The Th17 and Th1 cell populations in lymph nodes from these mice decreased and increased, respectively, whereas the percentage of regulatory T cells was unchanged. Interestingly, a lack of Ahr specifically in T cells significantly suppressed collagen-induced arthritis development, whereas Ahr deficiency in macrophages had no effect. These finding indicate that the development of experimental autoimmune arthritis depends on the presence of Ahr in T cells, and that Th1/Th17 balance may be particularly important for this process.
AB - The contributions of aryl hydrocarbon receptor (Ahr) to the pathogenesis of rheumatoid arthritis have not been elucidated. Here, we show that Ahr deficiency ameliorated collagen-induced arthritis, a mouse model of RA. Collagen-immunized Ahr KO mice showed decreased serum levels of such proinflammatory cytokines as IL-1β and IL-6. The Th17 and Th1 cell populations in lymph nodes from these mice decreased and increased, respectively, whereas the percentage of regulatory T cells was unchanged. Interestingly, a lack of Ahr specifically in T cells significantly suppressed collagen-induced arthritis development, whereas Ahr deficiency in macrophages had no effect. These finding indicate that the development of experimental autoimmune arthritis depends on the presence of Ahr in T cells, and that Th1/Th17 balance may be particularly important for this process.
KW - Autoimmunity
KW - Dioxin receptor
KW - Immune regulation
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U2 - 10.1073/pnas.1111786108
DO - 10.1073/pnas.1111786108
M3 - Article
C2 - 21825138
AN - SCOPUS:80052155367
SN - 0027-8424
VL - 108
SP - 14222
EP - 14227
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 34
ER -