CD69‐null mice protected from arthritis induced with anti‐type II collagen antibodies
K Murata, M Inami, A Hasegawa, S Kubo… - International …, 2003 - academic.oup.com
K Murata, M Inami, A Hasegawa, S Kubo, M Kimura, M Yamashita, H Hosokawa, T Nagao…
International immunology, 2003•academic.oup.comCD69, 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 …
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 …
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.
Oxford University Press