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首页> 外文期刊>Infection and immunity >Site-specific immunity to Leishmania major in SWR mice: the site of infection influences susceptibility and expression of the antileishmanial immune response.
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Site-specific immunity to Leishmania major in SWR mice: the site of infection influences susceptibility and expression of the antileishmanial immune response.

机译：SWR小鼠对利什曼原虫主要的位点特异性免疫：感染的位点会影响抗疟原虫免疫反应的易感性和表达。

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Inbred strains of mice usually develop either of two divergent patterns of infection in response to Leishmania major. Resistant mice, which develop self-limiting infections, respond immunologically with the activation of gamma interferon-secreting Th1 helper T cells, while nonhealing infections in susceptible mice are characterized by the proliferation of interleukin-4-secreting Th2 cells. Development of these divergent responses is dependent primarily on the strain of mouse infected, although factors such as the infective dose, species, and strain of parasite can also influence the degree of resistance. In this study, we show that a single mouse strain, SWR, can develop totally divergent patterns of infection depending on the site of parasite inoculation. Both SWR mice and highly susceptible BALB/c mice developed progressive, ultimately fatal disease when inoculated in the dorsal skin over the base of the tail. However, SWR mice infected in the hind footpad developed far less severe infections, which were for the most part controlled, whereas BALB/c mice infected in this site developed severe, nonhealing lesions. Production of gamma interferon and interleukin-4 and measurement of immunoglobulin E levels in serum were used to assess the degree of Th1 and Th2 cell activation in infected mice. Cytokine profiles early in infection had characteristics of a mixed Th1-Th2 response and were similar in SWR mice infected at either site. These early cytokine responses were not predictive of the ultimate disease outcome, since lymph node cells from healing mice eventually produced higher levels of gamma interferon than did those from nonhealing mice, and healing mice had lower levels of immunoglobulin E in serum, suggesting a functional bias toward Th1 cell activity in these animals. The differential ability of SWR mice to heal infections at different cutaneous sites provides a new model for the study of resistance to cutaneous leishmaniasis. Unlike traditional models of infection in which resistant and susceptible strains of mice are compared, this model allows for the study of factors that contribute to healing and nonhealing infections in a genetically identical strain of mouse.
机译：自交系小鼠通常会针对大利什曼原虫产生两种不同的感染模式。产生自限性感染的抗性小鼠通过分泌γ干扰素的Th1辅助T细胞的活化产生免疫反应，而易感小鼠中的非愈合感染则以分泌白细胞介素4的Th2细胞的增殖为特征。这些分歧反应的发生主要取决于感染的小鼠的品系，尽管诸如感染剂量，种类和寄生虫品系等因素也会影响抗药性。在这项研究中，我们显示了一个单一的小鼠品系，SWR，可以根据寄生虫接种的部位发展出完全不同的感染模式。当SWR小鼠和高度敏感的BALB / c小鼠接种在尾巴底部的背部皮肤中时，都会发展为进行性疾病，最终致命。但是，在后脚掌感染的SWR小鼠发生的感染严重程度要低得多，而大多数情况是可以控制的，而在该部位感染的BALB / c小鼠则发生了严重的，不愈合的病变。 γ干扰素和白细胞介素4的产生以及血清中免疫球蛋白E水平的测量被用于评估感染小鼠中Th1和Th2细胞活化的程度。感染初期的细胞因子谱具有混合的Th1-Th2反应特征，在任一部位感染的SWR小鼠中相似。这些早期的细胞因子反应不能预测最终的疾病结局，因为康复小鼠的淋巴结细胞最终产生的γ干扰素水平高于未治愈小鼠的淋巴结细胞，并且康复小鼠血清中的免疫球蛋白E水平较低，提示功能偏倚这些动物的Th1细胞活性。 SWR小鼠在不同皮肤部位治愈感染的差异能力为研究对皮肤利什曼病的耐药性提供了新模型。与传统的感染模型不同，在传统的感染模型中比较了小鼠的耐药和易感株，该模型允许研究在基因相同的小鼠株中有助于治愈和不治愈感染的因素。

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