Contribution of neutrophils in the pathogenesis of rheumatoid arthritis
被引:1
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作者:
Lingshu Zhang
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机构:
Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Department of Rheumatology and Immunology, the First Hospital of Jilin UniversityDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Lingshu Zhang
[1
,2
]
Yi Yuan
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h-index: 0
机构:
Rheumatology Section, VA Portland Healthcare SystemDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Yi Yuan
[3
]
Qiang Xu
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机构:
Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Department of Rheumatology and Immunology, the First Hospital of Jilin UniversityDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Qiang Xu
[1
,2
]
Zhengyu Jiang
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h-index: 0
机构:
Rheumatology Section, VA Portland Healthcare SystemDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Zhengyu Jiang
[3
]
Cong-Qiu Chu
论文数: 0引用数: 0
h-index: 0
机构:
Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Department of Rheumatology and Immunology, the First Hospital of Jilin UniversityDivision of Arthritis and Rheumatic Diseases, Oregon Health & Science University
Cong-Qiu Chu
[1
,2
]
机构:
[1] Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University
[2] Department of Rheumatology and Immunology, the First Hospital of Jilin University
[3] Rheumatology Section, VA Portland Healthcare System
Neutrophils are major innate immune effector cells for host defense and have been a topic of active research for their participation in the pathogenesis of autoimmune inflammatory diseases including rheumatoid arthritis(RA)due to recently discovered neutrophil extracellular trap(NET) formation. NET formation and other mechanisms leading to the release of neutrophil nuclear and cytoplasmic contents are implicated as a source of citrullinated antigens in RA. Further investigations are required to delineate what factors diverge neutrophils from host defense to autoimmune response in RA.