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首页> 外文期刊>Infection and immunity >Effect of antigen-specific T helper cells or interleukin-2 on suppressive ability of macrophage subsets detected in spleens of Trypanosoma cruzi-infected mice as determined by limiting dilution-partition analysis.
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Effect of antigen-specific T helper cells or interleukin-2 on suppressive ability of macrophage subsets detected in spleens of Trypanosoma cruzi-infected mice as determined by limiting dilution-partition analysis.

机译：抗原特异性T辅助细胞或白介素2对克氏锥虫感染小鼠脾脏中检测到的巨噬细胞亚群抑制能力的影响（通过有限稀释-分区分析确定）。

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Trypanosoma cruzi, a protozoan parasite and the causative agent of Chagas' disease, induces a state of lymphocyte hyporesponsiveness to both mitogenic and antigenic stimuli in mice during the acute phase of infection. Addition of spleen cells from T. cruzi-infected mice (SCinf) to microcultures of spleen cells from noninfected mice (SCn) suppresses the responsiveness of such cultures to antigenic challenge and to mitogenic stimulation. We analyzed the regulatory cell populations in SCinf by limiting dilution-partition analysis and found a complex regulatory circuit in T. cruzi-infected mice consisting of two suppressive macrophage subsets and an enhancing T-cell population. This T-cell population was able to abrogate or escape the suppressive ability of one suppressor macrophage subset, yet was suppressed by the other macrophage subset. To further study the cellular interactions of this regulatory circuit and analyze the suppressive abilities of the two suppressor macrophage subsets, we examined the effect of adding either primed T helper cells of known specificity or interleukin-2 to the limiting dilution-partition analysis microcultures. The results of these experiments suggest that one suppressor macrophage subset, which is abundant and, therefore, detected with low doses of SCinf, is able to suppress both mitogen- and primary antigen-specific responses but is unable to inhibit cells once they are already activated or primed. The other macrophage subset, which is presumably a less abundant or less active population (since high doses of SCinf are required to detect it), is able to suppress the response of activated or primed T cells by the inhibition of interleukin-2 production.
机译：克氏锥虫是一种原生动物的寄生虫，是恰加斯氏病的病原体，在感染的急性期可诱导小鼠对有丝分裂和抗原刺激的淋巴细胞反应低下。将来自克氏锥虫感染小鼠（SCinf）的脾细胞添加到未感染小鼠（SCn）的脾细胞的微培养物中，可以抑制这种培养物对抗原攻击和促有丝分裂刺激的响应。我们通过有限的稀释度分区分析法分析了SCinf中的调控细胞群，并发现在T. cruzi感染的小鼠中复杂的调控电路由两个抑制性巨噬细胞亚群和一个增强的T细胞群组成。该T细胞群能够消除或逃避一个抑制巨噬细胞亚群的抑制能力，但被另一巨噬细胞亚群抑制。为了进一步研究该调节回路的细胞相互作用并分析两个抑制巨噬细胞亚群的抑制能力，我们研究了将已知特异性的初免T辅助细胞或白介素2添加到有限稀释分区分析微培养物中的作用。这些实验的结果表明，一个丰富的抑制巨噬细胞亚群因此被低剂量的SCinf检测到，能够抑制促分裂原和主要抗原特异性反应，但是一旦被激活就无法抑制细胞。或灌注。其他的巨噬细胞亚群可能是数量较少或活性较低的种群（因为需要高剂量的SCinf才能检测到它），它能够通过抑制白介素2的产生来抑制活化的或引发的T细胞的应答。

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