中文摘要：

利用磁珠法分选野生型和FcγRIIb缺陷小鼠脾脏CD19＋B细胞,体外用LPS和/或FcγRIIb配体（IC）刺激24h后,流式细胞术（FCM）检测细胞表面共刺激分子的表达。用蛋白质印迹法检测IC刺激后B细胞内相关蛋白激酶的磷酸化情况。用Lyn抑制剂作用后,FCM检测LPS活化B细胞表面共刺激分子表达探讨B细胞内FcγRIIb对TLR4激动剂（LPS）诱导共刺激分子表达的影响。结果表明：IC抑制LPS活化B细胞表面CD40和CD80的表达,而在FcγRIIb缺陷小鼠B细胞内这一抑制作用消失。IC诱导B细胞内蛋白激酶Lyn的磷酸化,但不能诱导FcγRIIb缺陷小鼠B细胞内Lyn磷酸化。使用Lyn抑制剂后LPS活化B细胞表面CD40的表达上调。说明B细胞内FcγRIIb通过活化Lyn抑制TLR4激动剂诱导的CD40表达。

英文摘要：

Splenic B cells from wild type（WT）and FcγRIIb knockout mice were stimulated with LPS and/or FcγRIIb ligand（immune complex,IC）.After 24 h,cells were analyzed for costimulatory molecules expression by flow cytometry（FCM）.Western blot analysis was performed for phosphorylated protein kinases in lysates of splenic B cells stimulated with IC.FCM analysis was used for costimulatory molecules expression on splenic B cells pretreated with an inhibitor of Lyn,followed by LPS stimulation.Then,the effects of FcγRIIb on TLR4agonist（lipopolysaccharide,LPS）-induced costimulatory molecules expression in B cells were studied.showed that IC treatment inhibited CD40 and CD80expression on B cells stimulated with LPS.The inhibitory effect of IC on LPS-triggered CD40 and CD80expression was lost when B cells from FcγRIIb-/-mice were used.The phosphorylation of Lyn increased when WT B cells were stimulated with IC.However,the phosphorylation of Lyn showed a similar level when FcγRIIb-/-B cells were used.Furthermore,the inhibitor of Lyn enhanced the LPS-induced CD40 expression.FcγRIIb inhibits TLR4agonist-induced CD40 expression in B cells via activating Lyn.