Degradation of Cdc42 in response to lipid antigen variants controls immune responses of iNKT cells via regulating direction of IL4 secretion
作者单位：School of Life Sciences and Medical CenterUniversity of Science and Technology of China
会议名称：《第十二届全国免疫学学术大会》
会议日期：2017年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
关 键 词：iNKT polarization IL-4 Cdc42
摘 要：Invariant natural killer T(iNKT) cells which link innate immunity and adaptive immunity can rapidly produce both Th1 and Th2 cytokines in response to stimulus.However,Th1 or Th2 biased immune responses have been reported under certain conditions and the underlying mechanisms are not fully understood.Here,we demonstrated that lipid antigens inducing Th1 responses but not lipid variants inducing Th2 responses caused polarized secretion of IL4 at the immune synapses(IS).Accumulation of IL4 at synapses promoted IL12 production from dendritic cells(DCs),which in turn augmented IFNg production from iNKT cells.Comparing to polarized secretion,multi-directional secretion of IL4 induced by Th2 lipid variants dampened IL12 production from DCs,and thus,caused Th2 biased cytokine responses.The duration of polarized secretion was controlled by Cdc42,which was degraded by proteasomes in response to distinct TCR signaling.