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首页> 外文期刊>Infection and immunity >Th1 and Th2 cell-associated cytokines in experimental visceral leishmaniasis.
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Th1 and Th2 cell-associated cytokines in experimental visceral leishmaniasis.

机译：实验性内脏利什曼病中Th1和Th2细胞相关的细胞因子。

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In experimental Leishmania donovani infection in BALB/c mice, initial susceptibility gives way to T-cell-dependent acquired resistance and eventual control over visceral infection. Since various cytokines appear to underlie the host response to Leishmania infection, we examined infected liver tissue for gene expression of cytokines associated with Th1 (gamma interferon [IFN-gamma] and interleukin-2 [IL-2]) and Th2 cells (IL-4 and IL-10). By Northern (RNA) blot analysis, only IFN-gamma mRNA expression was detected in livers of infected euthymic mice. To determine whether activation of Th1 cells develops selectively in this model, qualitative PCR analysis was used. These results indicated that mRNAs for IFN-gamma, IL-2, IL-4, and IL-10 were all induced by L. donovani infection. The potentially negative Th2 cell-associated response did not appear to play a functional role, however, since resistance was acquired, anti-IL-4 monoclonal antibody treatment did not accelerate control over visceral infection, and serum immunoglobulin E levels remained low. As judged by PCR analysis, IL-4 and IL-10 mRNAs were also expressed under three other conditions without apparent effect: in naive euthymic mice treated with IL-2, which induces leishmanicidal activity; in rechallenged immune mice, which resist reinfection; and in nude mice, which fail to control L. donovani. These results suggest that, like other Leishmania species, L. donovani infection may trigger a potentially suppressive Th2 cell-associated cytokine response. However, in T-cell-intact mice able to control L. donovani, this response either is insufficient to influence outcome or more likely is overshadowed by the Th1 cell response.
机译：在BALB / c小鼠的实验性利什曼原虫donovani感染中，最初的敏感性被T细胞依赖性获得性耐药性所取代，并最终控制了内脏感染。由于各种细胞因子似乎是宿主对利什曼原虫感染的基础，因此我们检查了感染的肝组织中与Th1（γ干扰素[IFN-γ]和IL-2 [IL-2]）和Th2细胞（IL- 4和IL-10）。通过Northern（RNA）印迹分析，在感染的正常小鼠的肝脏中仅检测到IFN-γmRNA表达。为了确定在此模型中Th1细胞的激活是否选择性发展，使用了定性PCR分析。这些结果表明IFN-γ，IL-2，IL-4和IL-10的mRNA均由多诺氏乳杆菌感染诱导。潜在的与Th2细胞相关的阴性反应似乎没有发挥功能性作用，但是，由于获得了耐药性，抗IL-4单克隆抗体治疗不能促进对内脏感染的控制，并且血清免疫球蛋白E水平仍然较低。通过PCR分析判断，IL-4和IL-10 mRNA在其他三种条件下也没有明显作用表达：在用IL-2治疗的幼稚的正常小鼠中，其诱导了利什曼活性;在抵抗再感染的免疫小鼠中;以及无法控制多诺尼乳杆菌的裸鼠。这些结果表明，与其他利什曼原虫物种一样，多诺氏乳杆菌感染可能会触发潜在的抑制性Th2细胞相关细胞因子反应。但是，在能够控制多诺氏乳杆菌的T细胞完整小鼠中，这种反应要么不足以影响预后，要么更可能被Th1细胞反应所掩盖。

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