| First Author | Murata K | Year | 2003 |
| Journal | Int Immunol | Volume | 15 |
| Issue | 8 | Pages | 987-92 |
| PubMed ID | 12882836 | Mgi Jnum | J:84940 |
| Mgi Id | MGI:2670833 | Doi | 10.1093/intimm/dxg102 |
| Citation | Murata K, et al. (2003) CD69-null mice protected from arthritis induced with anti-type II collagen antibodies. Int Immunol 15(8):987-92 |
| abstractText | 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. |
