期刊
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY
卷 38, 期 6, 页码 445-449出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/03009740902895743
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资金
- American College of Rheumatology
- NIH [K08 AI070684-01]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [K08AI070684] Funding Source: NIH RePORTER
Objective: S100A8 (calgranulin A, MRP8) and S100A9 (calgranulin B, MRP14) are calcium-binding proteins highly expressed by activated myeloid cells and thought to be involved in the pathogenesis of inflammatory diseases. Circulating levels of S100A8/S100A9 are elevated in both human and experimental models of autoimmune disease, including rheumatoid arthritis (RA). Methods: Mice deficient in S100A9 (S100A9-/-) and wild-type controls were immunized using standard techniques for the K/BxN serum transfer or the collagen-induced arthritis (CIA) model. Results: S100A9-/- animals, with defective expression of both S100A8 and S100A9 proteins, had similar arthritis and histopathology to that of wild-type controls in both mouse models. Conclusion: S100A8 and S100A9 are not essential for disease expression in either the K/BxN serum transfer or the CIA model of inflammatory arthritis.
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