PGE2，外周成熟B细胞功能的新调控因子

Aim: Prostaglandin E2 is an important lipid substance, making effect through its EP1-4 receptors. PGE2 play an essential role in many systems. Out study focused on exploring PGE2's influence on peripheral mature B cells through EP2 receptor. Methods: Based on the study of EP2 knockout mice, the phynotype of splenic B cells was screened as well as the proliferation and apoptosis.Moreover, after hybriding EP2-/- mice with MRL/lpr mice, the initiation and accumulation of lupus-like syndromes was carefully examined in order to explore the influence of PGE2 on autoimmune disease mainly induced by B cells. Results: the deficiency of EP2 may make the spleen of knockout mice much larger than wild type mice and their splenic B cells accumulated abnormally.Furthermore, the activation marker such as CD62L and Bcl-2 were damatically changed on EP2-/- B cells. Accordingly, the proliferation of splenic B cells was significantly up-regulted and their apoptosis was down-regulated.After deleting EP2 receptor in MRL/lpr mice, the pathogenisis of lupus-like disease was obviously moved up, accompanying with far more severe of serum anti-self antibodies and kidney tissue destroy. Conclusion: Our data dropped a hint that PGE2 may be a negative regulator for B cells and the PGE2 signal through EP2 receptor would a protential effector in certain autoimmune disease. The result of our research would help to understand the activation and development of B cells better, broaden the cognition of PGE2's physiological effect, and may give a clue for a new medical interfere therapy.