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CD4+ T lymphocyte subsets express connexin 43 and establish gap junction channel communication with macrophages in vitro

机译:CD4 + T淋巴细胞亚群表达连接蛋白43并在体外与巨噬细胞建立间隙连接通道通讯

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摘要

Gap junction channels constructed of connexins (Cxs) are expressed by peripheral and secondary lymphoid organ-derived lymphocytes. These channels in the plasma membrane play key roles in a range of lymphocyte functions exemplified by the synthesis and secretion of Igs and cytokines and during transmigration across the endothelium. Most recently, their involvement in antigen cross-presentation has also been established. We report here for the first time the expression of mRNA and protein encoding Cx43 in mouse-derived CD4+ Th0, Th1, and Th2 lymphocyte subpopulations and demonstrate the establishment gap junction channel formation with primary macrophages in vitro. We show that this mode of direct communication is particularly favored in Th1-macrophage interactions and that LPS inhibits lymphocyte-macrophage cross-talk independently of the subset of lymphocyte involved. Our work suggests that gap junction-mediated communication can be modulated in the absence of specific antigenic stimulation. Therefore, a further mechanism featuring gap junction-mediated communication may be implicated in immune regulation.
机译:由连接蛋白(Cxs)构成的间隙连接通道由外周和继发性淋巴器官来源的淋巴细胞表达。质膜中的这些通道在一系列淋巴细胞功能中发挥关键作用,例如Igs和细胞因子的合成和分泌以及在跨内皮的迁移过程中。最近,还确定了它们参与抗原交叉呈递。本文首次报道了小鼠源性CD4 + Th0,Th1和Th2淋巴细胞亚群中编码Cx43的mRNA和蛋白的表达,并证明了与原代巨噬细胞在体外建立间隙连接通道的形成。我们表明,这种直接通信方式在Th1巨噬细胞相互作用中特别受青睐,并且LPS独立于所涉及的淋巴细胞子集抑制淋巴细胞-巨噬细胞的串扰。我们的工作表明,在缺乏特异性抗原刺激的情况下,间隙连接介导的通讯可以被调节。因此,以间隙连接介导的沟通为特征的其他机制可能与免疫调节有关。

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