Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis
Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by the presence of autoantibodies against citrullinated protein antigens and proinflammatory cytokines which cause chronic synovitis, bone erosion, and eventual deformity; however, the precise etiology of RA is unclear. In...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2018/8549329 |
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| author | Weiqian Chen Qin Wang Yini Ke Jin Lin |
| author_facet | Weiqian Chen Qin Wang Yini Ke Jin Lin |
| author_sort | Weiqian Chen |
| collection | DOAJ |
| description | Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by the presence of autoantibodies against citrullinated protein antigens and proinflammatory cytokines which cause chronic synovitis, bone erosion, and eventual deformity; however, the precise etiology of RA is unclear. In the early stage of RA, neutrophils migrate into the articular cavity, become activated, and exert their function in an inflammatory process, suggesting an essential role of neutrophils in the initial events contributing to the pathogenesis of RA. Solid evidence exists that supports the contribution of neutrophil extracellular traps (NETs) to the production of autoantibodies against citrullinated proteins which can trigger the immune reaction in RA. Concurrently, proinflammatory cytokines regulate the neutrophil migration, apoptosis, and NET formation. As a result, the inflammatory neutrophils produce more cytokines and influence other immune cells thereby perpetuating the inflammatory condition in RA. In this review, we summarize the advances made in improving our understanding of neutrophil migration, apoptosis, and NET formation in the presence of an RA inflammatory milieu. We will also discuss the most recent strategies in modulating the inflammatory microenvironment that have an impact on neutrophil function which may provide alternative novel therapies for RA. |
| format | Article |
| id | doaj-art-4f50a9958a7f40f1a48a23fb5ea130cd |
| institution | Kabale University |
| issn | 2314-8861 2314-7156 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-4f50a9958a7f40f1a48a23fb5ea130cd2025-02-03T06:12:28ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/85493298549329Neutrophil Function in an Inflammatory Milieu of Rheumatoid ArthritisWeiqian Chen0Qin Wang1Yini Ke2Jin Lin3Division of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, ChinaDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, ChinaDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, ChinaDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, ChinaRheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by the presence of autoantibodies against citrullinated protein antigens and proinflammatory cytokines which cause chronic synovitis, bone erosion, and eventual deformity; however, the precise etiology of RA is unclear. In the early stage of RA, neutrophils migrate into the articular cavity, become activated, and exert their function in an inflammatory process, suggesting an essential role of neutrophils in the initial events contributing to the pathogenesis of RA. Solid evidence exists that supports the contribution of neutrophil extracellular traps (NETs) to the production of autoantibodies against citrullinated proteins which can trigger the immune reaction in RA. Concurrently, proinflammatory cytokines regulate the neutrophil migration, apoptosis, and NET formation. As a result, the inflammatory neutrophils produce more cytokines and influence other immune cells thereby perpetuating the inflammatory condition in RA. In this review, we summarize the advances made in improving our understanding of neutrophil migration, apoptosis, and NET formation in the presence of an RA inflammatory milieu. We will also discuss the most recent strategies in modulating the inflammatory microenvironment that have an impact on neutrophil function which may provide alternative novel therapies for RA.http://dx.doi.org/10.1155/2018/8549329 |
| spellingShingle | Weiqian Chen Qin Wang Yini Ke Jin Lin Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis Journal of Immunology Research |
| title | Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis |
| title_full | Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis |
| title_fullStr | Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis |
| title_full_unstemmed | Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis |
| title_short | Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis |
| title_sort | neutrophil function in an inflammatory milieu of rheumatoid arthritis |
| url | http://dx.doi.org/10.1155/2018/8549329 |
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