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首页> 外文期刊>Infection and immunity >Cholera Toxin and Escherichia coli Heat-Labile Enterotoxin, but Not Their Nontoxic Counterparts, Improve the Antigen-Presenting Cell Function of Human B Lymphocytes
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Cholera Toxin and Escherichia coli Heat-Labile Enterotoxin, but Not Their Nontoxic Counterparts, Improve the Antigen-Presenting Cell Function of Human B Lymphocytes

机译：霍乱毒素和大肠杆菌的热不稳定肠毒素，但不是它们的无毒对应物，可改善人B淋巴细胞的抗原呈递细胞功能

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B lymphocytes play an important role in the immune response induced by mucosal adjuvants. In this study we investigated the in vitro antigen-presenting cell (APC) properties of human B cells upon treatment with cholera toxin (CT) and Escherichia coli heat-labile enterotoxin (LT) and nontoxic counterparts of these toxins, such as the B subunit of CT (CT-B) and the mutant of LT lacking ADP ribosyltransferase activity (LTK63). Furthermore, forskolin (FSK), a direct activator of adenylate cyclase, and cyclic AMP (cAMP) analogues were used to investigate the role of the increase in intracellular cAMP caused by the A subunit of CT and LT. B lymphocytes were cultured with adjuvants and polyclonal stimuli necessary for activation of B cells in the absence of CD4 T cells. Data indicated that treatment with CT, LT, FSK, or cAMP analogues, but not treatment with CT-B or LTK63, upregulated surface activation markers on B cells, such as CD86 and HLA-DR, and induced inhibition of the proliferation of B cells at early time points, while it increased cell death in long-term cultures. Importantly, B cells treated with CT, LT, or FSK were able to induce pronounced proliferation of both CD4+ and CD8+ allogeneic T cells compared with untreated B cells and B cells treated with CT-B and LTK63. Finally, only treatment with toxins or FSK induced antigen-specific T-cell proliferation in Mycobacterium tuberculosis purified protein derivative or tetanus toxoid responder donors. Taken together, these results indicated that the in vitro effects of CT and LT on human B cells are mediated by cAMP.
机译：B淋巴细胞在粘膜佐剂诱导的免疫反应中起重要作用。在这项研究中，我们研究了霍乱毒素（CT）和大肠杆菌不耐热肠毒素（LT）处理后人B细胞的体外抗原呈递细胞（APC）特性，以及它们的无毒对应物毒素，例如CT的B亚基（CT-B）和缺乏ADP核糖基转移酶活性的LT突变体（LTK63）。此外，使用了Forskolin（FSK）（腺苷酸环化酶的直接激活剂）和环状AMP（cAMP）类似物来研究由CT和LT的A亚基引起的细胞内cAMP升高的作用。在没有CD4 T细胞的情况下，将B淋巴细胞与佐剂和激活B细胞所需的多克隆刺激物一起培养。数据表明，用CT，LT，FSK或cAMP类似物治疗，但不使用CT-B或LTK63治疗，上调了B细胞的表面活化标记，例如CD86和HLA-DR，并诱导了对B细胞增殖的抑制在早期的时间点，虽然它增加了长期培养中的细胞死亡。重要的是，与未处理的B细胞和B细胞相比，经CT，LT或FSK处理的B细胞能够诱导CD4 + 和CD8 + 同种异体T细胞的明显增殖用CT-B和LTK63处理。最后，只有用毒素或FSK处理才能在结核分枝杆菌纯化的蛋白衍生物或破伤风类毒素应答者中诱导抗原特异性T细胞增殖。综上所述，这些结果表明CT和LT对人B细胞的体外作用是由cAMP介导的。

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