title: CD69-null mice protected from arthritis induced with anti-type II collagen antibodies.
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.
authors.affiliation: Department of Molecular Immunology and Medical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Murata
authors.forename: Masamichi
authors.initials: M
authors.lastname: Inami
authors.forename: Akihiro
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kubo
authors.forename: Motoko
authors.initials: M
authors.lastname: Kimura
authors.forename: Masakatsu
authors.initials: M
authors.lastname: Yamashita
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hosokawa
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Nagao
authors.forename: Kazuo
authors.initials: K
authors.lastname: Suzuki
authors.forename: Kahoko
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shinkai
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Koseki
authors.forename: Masaru
authors.initials: M
authors.lastname: Taniguchi
authors.forename: Steven F
authors.initials: SF
authors.lastname: Ziegler
authors.forename: Toshinori
authors.initials: T
authors.lastname: Nakayama
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000843:Ankle Joint / Q000378:metabolism / Q000473:pathology; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015703:Antigens, CD / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D001169:Arthritis, Experimental / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology; D018925:Chemokines / Q000235:genetics; D024043:Collagen Type II / Q000276:immunology*; D016207:Cytokines / Q000235:genetics; D005260:Female; D020869:Gene Expression Profiling; D006614:Hindlimb / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017403:In Situ Hybridization / Q000379:methods; D037181:Lectins, C-Type; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013864:Thioglycolates / Q000494:pharmacology; D000099192:CD69 Antigens
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018925:Chemokines; D024043:Collagen Type II; D016207:Cytokines; D037181:Lectins, C-Type; D008070:Lipopolysaccharides; D013864:Thioglycolates; D000099192:CD69 Antigens