4.0 Article

S100A9 is not essential for disease expression in an acute (K/BxN) or chronic (CIA) model of inflammatory arthritis

期刊

SCANDINAVIAN JOURNAL OF RHEUMATOLOGY
卷 38, 期 6, 页码 445-449

出版社

TAYLOR & FRANCIS LTD
DOI: 10.3109/03009740902895743

关键词

-

资金

  1. American College of Rheumatology
  2. NIH [K08 AI070684-01]
  3. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [K08AI070684] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.0
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据