Defective responsiveness of CD5+ B1 cells to lipopolysaccharide in cytokine production

N. Koide, A. Morikawa, Hiroyasu Ito, T. Sugiyama, F. Hassan, S. Islam, G. Tumurkhuu, I. Mori, T. Yoshida, T. Yokochi
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引用次数: 3

Abstract

Previously, we found that mouse TH2.52 cells possess the characteristic of CD5+ B1 cells and proliferate in response to lipopolysaccharide (LPS). The effect of LPS on cytokine production by TH2.52 B1 cells was studied. TH2.52 cells constitutively produced a small amount of tumor necrosis factor (TNF)-α and interleukin (IL)-6, and TNF-α and IL-6 production was markedly enhanced by LPS stimulation. Although interferon (IFN)-γ caused the production of various cytokines, such as IL-2, IL-4, IL-6 and TNF-α in TH2.52 cells, LPS did not cause the production of such cytokines. LPS did not induce IFN-β production in TH2.52 cells and TH2.52 cells lacked the expression of several molecules participating in the MyD88-independent pathway in LPS signaling. Defective responsiveness of TH2.52 B1 cells to LPS in cytokine production might be responsible for the failure of IFN-β production due to the lack of molecules participating in the MyD88-independent pathway.
细胞因子产生中CD5+ B1细胞对脂多糖的反应缺陷
先前,我们发现小鼠TH2.52细胞具有CD5+ B1细胞的特征,并在脂多糖(LPS)的作用下增殖。研究了LPS对TH2.52 B1细胞产生细胞因子的影响。TH2.52细胞组成性地产生少量肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6, LPS刺激显著增强TNF-α和IL-6的产生。虽然干扰素(IFN)-γ引起TH2.52细胞产生多种细胞因子,如IL-2、IL-4、IL-6和TNF-α,但LPS没有引起这些细胞因子的产生。LPS不诱导TH2.52细胞产生IFN-β, TH2.52细胞缺乏参与LPS信号通路中myd88独立通路的几个分子的表达。由于缺乏参与myd88独立通路的分子,TH2.52 B1细胞对LPS产生细胞因子的反应性缺陷可能是IFN-β产生失败的原因。
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