期刊
SEMINARS IN IMMUNOPATHOLOGY
卷 39, 期 4, 页码 385-393出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-017-0631-3
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资金
- NIAID NIH HHS [UM1 AI110557] Funding Source: Medline
The profound alterations in the structure, cellular composition, and function of synovial tissue in rheumatoid arthritis (RA) are the basis for the persistent inflammation and cumulative joint destruction that are hallmarks of this disease. In RA, the synovium develops characteristics of a tertiary lymphoid organ, with extensive infiltration of lymphocytes and myeloid cells. Concurrently, the fibroblast-like synoviocytes undergo massive hyperplasia and acquire a tissue-invasive phenotype. In this review, we summarize key components of these processes, focusing on recently-described roles of selected molecular markers of these cellular components of RA synovitis.
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