Open AccessCCR6 controls autoimmune but not innate immunity‐driven experimental arthritis
Author(s) -
Bonelli Michael,
Puchner Antonia,
Göschl Lisa,
Hayer Silvia,
Niederreiter Birgit,
Steiner Guenter,
Tillmann Katharina,
Plasenzotti Roberto,
Podesser Bruno,
Georgel Philippe,
Smolen Josef,
Scheinecker Clemens,
Blüml Stephan
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13783
Subject(s) - arthritis , c c chemokine receptor type 6 , immunology , rheumatoid arthritis , chemokine , innate immune system , medicine , acquired immune system , inflammation , chemokine receptor , immune system
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease, characterized by synovial infiltration of various inflammatory cells. Chemokines are involved in controlling the recruitment of different cell types into the synovial membrane. The role of CCR6 in the development of arthritis so far remains unclear. In this study, we investigated the role of CCR6 in the pathogenesis of arthritis using three different murine arthritis models. Compared to WT animals, CCR6 −/− mice developed less clinical signs of arthritis in the collagen‐induced arthritis model but not in the K/BxN serum transfer arthritis model and in the human tumour necrosis factor transgenic arthritis model, suggesting a defect in adaptive effector functions but intact innate effector functions in the development of arthritis in CCR6 −/− animals. In line with this, anti‐collagen antibody levels were significantly reduced in CCR6 −/− mice compared with WT mice. Moreover, we demonstrate enhanced osteoclastogenesis in vitro in CCR6 −/− mice compared with WT mice. However, we did not detect differences in bone mass under steady state conditions in vivo between WT and CCR6‐deficient mice. These data suggest that CCR6 is crucially involved in adaptive but not in innate immunity‐driven arthritis. CCR6 or its chemokine ligand CCL20 might represent a possible new target for the treatment of RA.