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International Immunology, Vol. 15, No. 8, pp. 987-992, August 2003
© 2003 Japanese Society for Immunology

FEATURED ARTICLE OF THE MONTH

CD69-null mice protected from arthritis induced with anti-type II collagen antibodies

Kaoru Murata1,2, Masamichi Inami1, Akihiro Hasegawa1, Shuichi Kubo1, Motoko Kimura1, Masakatsu Yamashita1,4, Hiroyuki Hosokawa1, Tomokazu Nagao7, Kazuo Suzuki7, Kahoko Hashimoto5, Hiroshi Shinkai2, Haruhiko Koseki3, Masaru Taniguchi1,6, Steven F. Ziegler8 and Toshinori Nakayama1

Departments of 1 Molecular Immunology and Medical Immunology, 2 Clinical Biology of Extracellular Matrix and 3 Molecular Embryology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan 4 PRESTO, Japan Science and Technology Corp., 5 Laboratory for Dendritic Cell Immunobiology and 6 Laboratory for Immune Regulation, RIKEN Research Center for Allergy and Immunology, Japan 7 Biodefense Laboratory, Department of Bioactive Molecule, National Institute of Infectious Diseases, Tokyo 162-8640, Japan 8 Immunology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA 98101, USA

Correspondence to: T. Nakayama; E-mail: nakayama{at}med.m.chiba-u.ac.jp
Transmitting editor: M. Miyasaka

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


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