CXCL13 neutralization reduces the severity of collagen-induced arthritis
| Autor: | Swanthri De Silva, Biao Zheng, Linjie Guo, Daniel Wansley, Michael R. West, Zeynep Ozen, David P. Huston, Shuhua Han, Ekaterina Marinova, Xuejun Zhang |
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| Rok vydání: | 2005 |
| Předmět: |
Male
musculoskeletal diseases T-Lymphocytes medicine.medical_treatment Immunology Arthritis Spleen macromolecular substances Lymphocyte proliferation Antibodies Mice Immune system Rheumatology Neutralization Tests medicine Animals Immunology and Allergy Pharmacology (medical) CXCL13 Collagen Type II Autoimmune disease biology business.industry Synovial Membrane medicine.disease Arthritis Experimental Chemokine CXCL13 Interleukin-10 medicine.anatomical_structure Cytokine Mice Inbred DBA biology.protein Cytokines Antibody business Chemokines CXC |
| Zdroj: | Arthritis & Rheumatism. 52:620-626 |
| ISSN: | 1529-0131 0004-3591 |
| DOI: | 10.1002/art.20768 |
| Popis: | Objective To investigate the role of CXCL13 in the development and pathogenesis of collagen-induced arthritis (CIA), and to determine the mechanisms involved in the modulation of arthritogenic response by CXCL13 neutralization. Methods Mice were immunized with type II collagen (CII) and treated with anti-CXCL13 or control antibodies during boosting. Mice were monitored for the development and severity of arthritis. The effects of CXCL13 neutralization on immune response to CII were evaluated by cytokine production by CII-specific T cells and CII-specific antibody production. Follicular response in the spleen and in synovial tissue was determined by in situ immunohistology. Results Mice receiving neutralizing antibodies to CXCL13 developed significantly less severe arthritis compared with mice injected with phosphate buffered saline or control antibodies. Follicular response both in the spleen and in synovial tissue was inhibited by anti-CXCL13 treatment. Injection with anti-CXCL13 antibodies did not significantly affect antigen-specific recall lymphocyte proliferation or type 1 cytokine production in vitro. Antibody response specific to CII was not inhibited by anti-CXCL13 treatment. However, anti-CXCL13 treatment induced significantly higher levels of interleukin-10 production after in vitro CII stimulation. Conclusion Neutralization of CXCL13 inhibits the development of CIA and reduces follicular response in both lymphoid and nonlymphoid tissues. These findings may have important implications regarding the pathogenesis and treatment of autoimmune arthritis. |
| Databáze: | OpenAIRE |
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