tailieunhanh - Báo cáo khoa học: " A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior"

A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior | Zhang et al. Virology Journal 2010 7 30 http content 7 1 30 VIROLOGY JOURNAL HYPOTHESIS Open Access A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior 1 f 11 1Ỷ . 2 1 1 1 3 Chuanfu Zhang Yuanyong Xu Leili Jia Yutao Yang Yong Wang Yansong Sun Liuyu Huang Fei Qiao Stephen Tomlinson3 Xuelin Liu1 Yusen Zhou4 Hongbin Song1 Abstract Background Influenza is a respiratory disease that seriously threatens human health. In fact influenza virus itself does not make critical contribution to mortality induced by influenza but cytokine storm produced by the excessive immune response triggered by the virus can result in inflammatory reaction of lung tissues and fatal lung tissue injury and thus increase influenza mortality. Therefore besides antiviral drugs immunosuppression drugs should also be included in infection treatment. Presentation of the hypothesis Complement is the center of inflammatory reaction. If complement system is over activated the body will have strong inflammatory reaction or tissue injury resulting in pathological process. Many studies have proved that inflammatory injury of lung tissues caused by influenza virus is closely related to complement activation. Therefore inhibiting complement activation can significantly reduce inflammatory injury in lung tissues. As complement is both a physiological defense and pathological damage medium systematic inhibition may result in side effects including infection. Therefore we design targeting complement inhibitors for complement activation sites . with CR2 as targeting vector complement inhibitors like CD59 and Crry are targeted to inflammatory sites to specially inhibit the complement activation in local injury thus local inflammatory reaction is inhibited. Testing the hypothesis CR2-CD59 and CR2-Crry targeting complement inhibitors are fusion-expressed and their biological activity is examined via in vivo and in vitro tests. CR2 .