Search

Your search keyword '"Ayako Takaki-Kuwahara"' showing total 2 results
Start Over Author "Ayako Takaki-Kuwahara"
2 results on '"Ayako Takaki-Kuwahara"'

1. CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines

Author

Ayako Takaki-Kuwahara, Yojiro Arinobu, Kohta Miyawaki, Hisakata Yamada, Hirofumi Tsuzuki, Kensuke Irino, Masahiro Ayano, Yasutaka Kimoto, Hiroki Mitoma, Mitsuteru Akahoshi, Hiroshi Tsukamoto, Takahiko Horiuchi, Hiroaki Niiro, and Koichi Akashi

Subjects
Innate lymphoid cells, Rheumatoid arthritis, CCR6, Th17 cytokines, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA). Methods In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients. Results In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p

Published
2019
Full Text
View/download PDF

2. CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines

Author

Hirofumi Tsuzuki, Hisakata Yamada, Hiroki Mitoma, Ayako Takaki-Kuwahara, Hiroaki Niiro, Mitsuteru Akahoshi, Yojiro Arinobu, Koichi Akashi, Kensuke Irino, Hiroshi Tsukamoto, Takahiko Horiuchi, Yasutaka Kimoto, Masahiro Ayano, and Kohta Miyawaki

Subjects
Male, Receptors, CCR6, 0301 basic medicine, medicine.medical_specialty, lcsh:Diseases of the musculoskeletal system, Arthritis, Innate lymphoid cells, Inflammation, C-C chemokine receptor type 6, Th17 cytokines, Arthritis, Rheumatoid, Mice, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Synovial Fluid, Animals, Humans, Medicine, Synovial fluid, Rheumatoid arthritis, skin and connective tissue diseases, 030203 arthritis & rheumatology, business.industry, Interleukin-17, Innate lymphoid cell, medicine.disease, Immunity, Innate, Rheumatology, Mice, Inbred C57BL, CCL20, Disease Models, Animal, 030104 developmental biology, Gene Expression Regulation, Immunology, Disease Progression, RNA, Th17 Cells, lcsh:RC925-935, medicine.symptom, CCR6, business, Research Article
Abstract

Background Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA). Methods In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients. Results In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results