IL-1β通过诱导TLR4表达增强协同LPS刺激引起的狼疮小鼠B细胞的功能异常

IL-1β synergistically strengthen the LPS-induced dysfunction of B cells from SLE mice by up-regulation of TLR4 expression

目的:探索IL-1β对SLE模型小鼠脾脏B细胞功能的影响。方法:磁珠分选纯化正常小鼠及SLE模型小鼠脾脏B细胞。用不同浓度的IL-1β或LPS联合IL-1β处理分选的B细胞后,CCK8检测B细胞增殖情况,流式细胞仪检测B细胞的活化及TLR4的表达,实时定量PCR方法分析细胞因子的表达。结果:获得的B细胞纯度高达95%。IL-1β不影响正常小鼠和SLE小鼠脾脏B细胞的增殖,也不影响共刺激分子CD80和CD86的表达。但IL-1β可上调SLE小鼠B细胞中CD40、CD69、IL-6及IL-10的表达。进一步,IL-1β与LPS协同可增强SLE小鼠B细胞的CD40及CD69表达。IL-1β还可上调SLE小鼠B细胞中TLR4的表达。结论:IL-1β可能通过诱导TLR4表达来增强LPS刺激引起的SLE小鼠的B细胞功能异常,提示控制感染和抑制炎症可能达到减缓SLE病程的目的。

Objective：To explore the effect of IL-1β on function of B cells obtained from SLE mouse spleen in vitro.Methods：B cells were sorted from spleen of both normal and SLE mice using magnetic bead.After treatment of IL-1β combined with or without LPS,proliferation of B cells was tested by CCK8-kit;activation of B cells and expression of TLR4 were checked by FCM;the expression of cytokines was examined by real time PCR.Results：The purity of sorted B cells was over 95%.IL-1β influenced neither the proliferation nor the expression of CD80 and CD86 of B cells from both normal and SLE mice,while IL-1β could up-regulate the expression of CD40,CD69,IL-6 and IL-10 in B cells from SLE mice.Moreover,IL-1β and LPS could synergistically strengthen the expression of CD40 and CD69 in B cells from SLE mice.Furthermore,IL-1β up-regulated the expression of TLR4 in B cells from SLE mice.Conclusion：IL-1β may strengthen the dysfunction of LPS-induced B cells from SLE mice through up-regulation of TLR4 expression.This suggests the prevention of infection and inhibition of inflammation may ameliorate SLE progression.