Eri Hayashi1, Asako Chiba2, Kurisu Tada1, Keiichi Haga1, Mie Kitagaichi1, Shihoko Nakajima1, Makio Kusaoi1, Fumio Sekiya1, Michihiro Ogasawara1, Ken Yamaji1, Naoto Tamura1, Yoshinari Takasaki1, Sachiko Miyake2. 1. From the Department of Internal Medicine and Rheumatology, and Department of Immunology, and Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.E. Hayashi, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; A. Chiba, MD, PhD, Department of Immunology, Juntendo University School of Medicine; K. Tada, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; K. Haga, MD, PhD, Department of Gastroenterology, Juntendo University School of Medicine; M. Kitagaichi, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; S. Nakajima, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; M. Kusaoi, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; F. Sekiya, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; M. Ogasawara, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; K. Yamaji, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; N. Tamura, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; Y. Takasaki, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; S. Miyake, MD, PhD, Department of Immunology, Juntendo University School of Medicine. 2. From the Department of Internal Medicine and Rheumatology, and Department of Immunology, and Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.E. Hayashi, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; A. Chiba, MD, PhD, Department of Immunology, Juntendo University School of Medicine; K. Tada, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; K. Haga, MD, PhD, Department of Gastroenterology, Juntendo University School of Medicine; M. Kitagaichi, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; S. Nakajima, MD, Department of Internal Medicine and Rheumatology, and Department of Immunology, Juntendo University School of Medicine; M. Kusaoi, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; F. Sekiya, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; M. Ogasawara, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; K. Yamaji, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; N. Tamura, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; Y. Takasaki, MD, PhD, Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine; S. Miyake, MD, PhD, Department of Immunology, Juntendo University School of Medicine. s-miyake@juntendo.ac.jp a-chiba@juntendo.ac.jp.
Abstract
OBJECTIVE: Ankylosing spondylitis (AS) is characterized by chronic inflammation of the axial and peripheral joints and ligamentous attachments. Gut immunity is thought to be involved in AS, because a prominent coexistence of gut and joint inflammation has been observed in patients with AS. Mucosal-associated invariant T (MAIT) cells are preferentially located in the gut lamina propria and produce inflammatory cytokines such as interleukin 17 (IL-17) and tumor necrosis factor-α (TNF-α), which are therapeutic targets for AS. This study aimed to investigate the involvement of MAIT cells in AS. METHODS: The frequency of MAIT cells and their cytokine production were determined in patients with AS and healthy controls (HC). The expression of a MAIT cell activation marker (CD69) was analyzed in patients with AS by using flow cytometry. RESULTS: The frequency of MAIT cells in the peripheral blood was lower in patients with AS compared with HC. The levels of IL-17 produced by MAIT cells after activation were higher in patients with AS than in the HC. CD69 expression on MAIT cells correlated with the Ankylosing Spondylitis Disease Activity Score in patients with AS. CONCLUSION: These results suggest the involvement of MAIT cells in the pathogenesis of AS.
OBJECTIVE:Ankylosing spondylitis (AS) is characterized by chronic inflammation of the axial and peripheral joints and ligamentous attachments. Gut immunity is thought to be involved in AS, because a prominent coexistence of gut and joint inflammation has been observed in patients with AS. Mucosal-associated invariant T (MAIT) cells are preferentially located in the gut lamina propria and produce inflammatory cytokines such as interleukin 17 (IL-17) and tumor necrosis factor-α (TNF-α), which are therapeutic targets for AS. This study aimed to investigate the involvement of MAIT cells in AS. METHODS: The frequency of MAIT cells and their cytokine production were determined in patients with AS and healthy controls (HC). The expression of a MAIT cell activation marker (CD69) was analyzed in patients with AS by using flow cytometry. RESULTS: The frequency of MAIT cells in the peripheral blood was lower in patients with AS compared with HC. The levels of IL-17 produced by MAIT cells after activation were higher in patients with AS than in the HC. CD69 expression on MAIT cells correlated with the Ankylosing Spondylitis Disease Activity Score in patients with AS. CONCLUSION: These results suggest the involvement of MAIT cells in the pathogenesis of AS.
Authors: Vidya Ranganathan; Eric Gracey; Matthew A Brown; Robert D Inman; Nigil Haroon Journal: Nat Rev Rheumatol Date: 2017-04-27 Impact factor: 20.543
Authors: Charles Kyriakos Vorkas; Matthew F Wipperman; Kelin Li; James Bean; Shakti K Bhattarai; Matthew Adamow; Phillip Wong; Jeffrey Aubé; Marc Antoine Jean Juste; Vanni Bucci; Daniel W Fitzgerald; Michael S Glickman Journal: JCI Insight Date: 2018-10-04