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IL-33 induces neutrophil migration in rheumatoid arthritis and is a target of anti-TNF therapy
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IL-33 induces neutrophil migration in rheumatoid arthritis and is a target of anti-TNF therapy
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Journal Article
IL-33 induces neutrophil migration in rheumatoid arthritis and is a target of anti-TNF therapy
2010
Overview
Objectives Interleukin 33 (IL-33) is a new member of the IL-1 family of cytokines which signals via its receptor, ST2 (IL-33R), and has an important role in Th2 and mast cell responses. This study shows that IL-33 orchestrates neutrophil migration in arthritis. Methods and results Methylated bovine serum albumin (mBSA) challenge in the knee joint of mBSA-immunised mice induced local neutrophil migration accompanied by increased IL-33R and IL-33 mRNA expression. Cell migration was inhibited by systemic and local treatments with soluble (s)IL-33R, an IL-33 decoy receptor, and was not evident in IL-33R-deficient mice. IL-33 injection also induced IL-33R-dependent neutrophil migration. Antigen- and IL-33-induced neutrophil migration in the joint was dependent on CXCL1, CCL3, tumour necrosis factor α (TNFα) and IL-1β synthesis. Synovial tissue, macrophages and activated neutrophils expressed IL-33R. IL-33 induces neutrophil migration by activating macrophages to produce chemokines and cytokines and by directly acting on neutrophils. Importantly, neutrophils from patients with rheumatoid arthritis successfully treated with anti-TNFα antibody (infliximab) expressed significantly lower levels of IL-33R than patients treated with methotrexate alone. Only neutrophils from patients treated with methotrexate alone or from normal donors stimulated with TNFα responded to IL-33 in chemotaxis. Conclusions These results suggest that suppression of IL-33R expression in neutrophils, preventing IL-33-induced neutrophil migration, may be an important mechanism of anti-TNFα therapy of inflammation.
Publisher
BMJ Publishing Group Ltd and European League Against Rheumatism,BMJ Publishing Group,Elsevier Limited
Subject
/ Antigens
/ Antirheumatic Agents - pharmacology
/ Arthritis, Experimental - drug therapy
/ Arthritis, Experimental - immunology
/ Arthritis, Rheumatoid - drug therapy
/ Arthritis, Rheumatoid - immunology
/ Biological and medical sciences
/ Chemotactic Factors - immunology
/ Chemotaxis, Leukocyte - immunology
/ Diseases of the osteoarticular system
/ Gene Expression Regulation - immunology
/ Humans
/ Interleukin-1 Receptor-Like 1 Protein
/ Macrophage Activation - immunology
/ Mice
/ Neutrophil Infiltration - immunology
/ Studies
/ Synovial Membrane - immunology
