Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model.

Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. Research Abstract Details 

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Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. Abstract Text:

Keiji Hirota,Hiroyuki Yoshitomi,Motomu Hashimoto,Shinji Maeda,Shin Teradaira,Naoshi Sugimoto,Tomoyuki Yamaguchi,Takashi Nomura,Hiromu Ito,Takashi Nakamura,Noriko Sakaguchi,Shimon Sakaguchi,Keiji Hirota,Hiroyuki Yoshitomi,Motomu Hashimoto,Shinji Maeda,Shin Teradaira,Naoshi Sugimoto,Tomoyuki Yamaguchi,Takashi Nomura,Hiromu Ito,Takashi Nakamura,Noriko Sakaguchi,Shimon Sakaguchi,

This report shows that interleukin (IL) 17-producing T helper type 17 (Th17) cells predominantly express CC chemokine receptor (CCR) 6 in an animal model of rheumatoid arthritis (RA). Th17 cells induced in vivo in normal mice via homeostatic proliferation similarly express CCR6, whereas those inducible in vitro by transforming growth factor beta and IL-6 additionally need IL-1 and neutralization of interferon (IFN) gamma and IL-4 for CCR6 expression. Forced expression of RORgamma t, a key transcription factor for Th17 cell differentiation, induces not only IL-17 but also CCR6 in naive T cells. Furthermore, Th17 cells produce CCL20, the known ligand for CCR6. Synoviocytes from arthritic joints of mice and humans also produce a large amount of CCL20, with a significant correlation (P = 0.014) between the amounts of IL-17 and CCL20 in RA joints. The CCL20 production by synoviocytes is augmented in vitro by IL-1beta, IL-17, or tumor necrosis factor alpha, and is suppressed by IFN-gamma or IL-4. Administration of blocking anti-CCR6 monoclonal antibody substantially inhibits mouse arthritis. Thus, the joint cytokine milieu formed by T cells and synovial cells controls the production of CCL20 and, consequently, the recruitment of CCR6+ arthritogenic Th17 cells to the inflamed joints. These results indicate that CCR6 expression contributes to Th17 cell function in autoimmune disease, especially in autoimmune arthritis such as RA.

Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. Publishing Authors By Initials

K Hirota,H Yoshitomi,M Hashimoto,S Maeda,S Teradaira,N Sugimoto,T Yamaguchi,T Nomura,H Ito,T Nakamura,N Sakaguchi,S Sakaguchi,K Hirota,H Yoshitomi,M Hashimoto,S Maeda,S Teradaira,N Sugimoto,T Yamaguchi,T Nomura,H Ito,T Nakamura,N Sakaguchi,S Sakaguchi,

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Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of experimental medicine

VOLUME: 204

Page Numbers: 2803-12

Journal Abbreviation: J. Exp. Med.

ISSN: 1540-9538

DAY: 19

MONTH: 11

YEAR: 2007

Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. Information

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LANGUAGE: eng

NlmUniqueID: 2985109

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Grant and Affiliation Information for Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model.

AFFILIATION: Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.

Country: United States

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MEDLINETA: J Exp Med

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