首页 | 本学科首页   官方微博 | 高级检索  
     


CD69-null mice protected from arthritis induced with anti-type II collagen antibodies
Authors:Murata Kaoru  Inami Masamichi  Hasegawa Akihiro  Kubo Shuichi  Kimura Motoko  Yamashita Masakatsu  Hosokawa Hiroyuki  Nagao Tomokazu  Suzuki Kazuo  Hashimoto Kahoko  Shinkai Hiroshi  Koseki Haruhiko  Taniguchi Masaru  Ziegler Steven F  Nakayama Toshinori
Affiliation:Department of Molecular Immunology and Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Abstract:CD69, known as an early activation marker antigen on T and B cells, is also expressed on platelets and activated neutrophils, suggesting certain roles in inflammatory diseases. In order to address the role of CD69 in the pathogenesis of arthritis, we established CD69-null mice. CD69-null mice displayed a markedly attenuated arthritic inflammatory response when injected with anti-type II collagen antibodies. Cell transfer experiments with neutrophils, but not T cells or spleen cells, from wild-type mice into CD69-null mice restored the induction of arthritis. These results indicate a critical role for CD69 in neutrophil function in arthritis induction during the effector phase. Thus, CD69 would be a possible therapeutic target for arthritis in human patients.
Keywords:IL-6   neutrophil   rheumatoid arthritis
本文献已被 PubMed Oxford 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号