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Udgivet

Protective Role of Collectin 11 in a Mouse Model of Rheumatoid Arthritis

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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  • Na Wang
  • Weiju Wu
  • Cui Qiang
  • Ning Ma
  • Kunyi Wu
  • Dan Liu
  • Jia-Xing Wang
  • Xiao Yang
  • Li Xue
  • Teng-Yue Diao
  • Jia-Yu Liu
  • Ang Li
  • Baojun Zhang
  • Zong-Fang Li
  • Conrad A Farrar
  • Nirmal K Banda
  • Rafael Bayarri-Olmos
  • Peter Garred
  • Wuding Zhou
  • Ke Li
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OBJECTIVE: Collectin 11 (CL-11) is a soluble C-type lectin, a mediator of innate immunity. Its role in autoimmune disorders is unknown. We undertook this study to determine the role of CL-11 in a mouse model of rheumatoid arthritis (RA).

METHODS: A murine collagen-induced arthritis (CIA) model was used and combined two approaches, including gene deletion of Colec11 and treatment with recombinant CL-11 (rCL-11). Joint inflammation and tissue destruction, circulating levels of inflammatory cytokines, and adaptive immune responses were assessed in mice with CIA. Splenic CD11c+ cells were used to examine the influence of CL-11 on antigen-presenting cell (APC) function. Serum CL-11 levels in RA patients were also examined.

RESULTS: Colec11-/- mice developed more severe arthritis than wild-type mice, as determined by disease incidence, clinical arthritis scores, and histopathology (P < 0.05). Disease severity was associated with significantly enhanced APC activation, Th1/Th17 responses, pathogenic IgG2a production and joint inflammation, as well as elevated circulating levels of inflammatory cytokines. In vitro analysis of CD11c+ cells revealed that CL-11 is critical for suppression of APC activation and function. Pharmacologic treatment of mice with rCL-11 reduced the severity of CIA in mice. Analysis of human blood samples revealed that serum CL-11 levels were lower in RA patients (n = 51) compared to healthy controls (n = 53). Reduction in serum CL-11 was inversely associated with the Disease Activity Score in 28 joints, erythrocyte sedimentation rate, and C-reactive protein level (P < 0.05).

CONCLUSION: Our findings demonstrate a novel role of CL-11 in protection against RA, suggesting that the underlying mechanism involves suppression of APC activation and subsequent T cell responses.

OriginalsprogEngelsk
TidsskriftArthritis and Rheumatology
Vol/bind73
Udgave nummer8
Sider (fra-til)1430-1440
Antal sider11
ISSN2326-5191
DOI
StatusUdgivet - aug. 2021

Bibliografisk note

© 2021 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.

ID: 72503071