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首页> 外文期刊>Infection and immunity >Complement Receptor 3 Deficiency Influences Lesion Progression during Leishmania major Infection in BALB/c Mice
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Complement Receptor 3 Deficiency Influences Lesion Progression during Leishmania major Infection in BALB/c Mice

机译：补体受体3缺乏影响BALB / c小鼠利什曼原虫大感染期间病变进展。

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摘要

Leishmania major is an obligately intracellular protozoan parasite that causes cutaneous leishmaniasis. Like numerous intracellular pathogens, Leishmania exploits cell surface receptors as a means of entry into host cells. Complement receptor 3 (CR3; also called CD11b/CD18), a β2 integrin on phagocytic cells, is one such receptor. Ligation of CR3 has been shown to inhibit the production of interleukin-12, the cytokine that is pivotal in establishing the cell-mediated response necessary to combat intracellular infection. Here we investigate the role that CR3 plays in the establishment and progression of cutaneous leishmaniaisis in vivo. Dermal lesions of wild-type BALB/c mice are characteristically progressive and lead to extensive tissue necrosis coupled with elevated parasite burdens; CD11b-deficient BALB/c mice, however, demonstrate an intermediate phenotype characterized by chronic lesions and a reduced incidence of tissue damage. Infection followed by a reinfection challenge indicates that both susceptible (BALB/c) and resistant (C57BL/6) mice, regardless of CD11b status, develop resistance to L. major. In addition, CD11b does not bias the T helper cytokine response to L. major infection. Our results further indicate that CD11b is not necessary for disease resolution in resistant mice; rather, this protein appears to play a minor role in susceptibility.
机译： Leishmania major 是专一的细胞内原生动物寄生虫，可引起皮肤利什曼病。像许多细胞内病原体一样，利什曼原虫利用细胞表面受体作为进入宿主细胞的一种手段。补体受体3（CR3;也称为CD11b / CD18）是吞噬细胞上的一种β 2 整合素。 CR3的连接已显示抑制白介素12的产生，白细胞介素12在建立对抗细胞内感染所必需的细胞介导的反应中至关重要。在这里，我们调查CR3在体内皮肤利什曼原虫的建立和进展中所起的作用。野生型BALB / c小鼠的皮肤病变特征性地进行性发展，并导致广泛的组织坏死和寄生虫负担增加;但是，缺乏CD11b的BALB / c小鼠表现出以慢性病变为特征的中间表型，并且组织损伤的发生率降低。感染后再感染，表明无论CD11b处于何种状态，易感（BALB / c）和耐药（C57BL / 6）小鼠均产生对 L的耐药性。主要。此外，CD11b不会使T辅助细胞因子对L的应答偏倚。严重的感染。我们的结果进一步表明，CD11b对于抗药性小鼠的疾病缓解不是必需的。相反，这种蛋白质似乎在易感性中起次要作用。

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