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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >The role of macrophage inflammatory protein-1 alpha/CCL3 in regulation of T cell-mediated immunity to Cryptococcus neoformans infection.
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The role of macrophage inflammatory protein-1 alpha/CCL3 in regulation of T cell-mediated immunity to Cryptococcus neoformans infection.

机译：巨噬细胞炎性蛋白-1 alpha / CCL3在调节T细胞介导的对新型隐球菌感染的免疫中的作用。

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摘要

Macrophage inflammatory protein-1alpha (MIP-1alpha/CCL3) is a CC chemokine required for optimal recruitment of leukocytes in response to cryptococcal Ags. MIP-1alpha is expressed in the lungs by day 6 post Cryptococcus neoformans infection and could play a role in the development of cell-mediated immunity. To address this possibility, wild-type (MIP-1alpha(+/+)) mice and MIP-1alpha knockout (MIP-1alpha(-/-)) mice were infected intratracheally with a highly virulent strain of C. neoformans (145A). MIP-1alpha message was detected in the lungs on days 3, 7, and 14 in MIP-1alpha(+/+) mice, but it was undetectable in MIP-1alpha(-/-) mice. On day 16, MIP-1alpha(-/-) mice had a 7-fold increase in C. neoformans burden in the lungs, but no decrease in pulmonary leukocyte recruitment. MIP-1alpha(+/+) and MIP-1alpha(-/-) mice had similar numbers of recruited lymphocytes and monocytes/macrophages. Notably, MIP-1alpha(-/-) mice had a significantly greater number of eosinophils. MIP-1alpha(-/-) mice had extremely high levels of serum IgE. This switch of immune response to a T(2) phenotype was associated with enhanced IL-4 and IL-13 expression in the lungs of MIP-1alpha(-/-) mice compared with MIP-1alpha (+/+) mice. Progression of pulmonary cryptococcosis in the presence of nonprotective T(2) immunity resulted in profound lung damage in MIP-1alpha(-/-) mice (eosinophilic crystal deposition, destruction of lung parenchyma, and pulmonary hemorrhage). Twelve-week survival was dramatically decreased in MIP-1alpha(-/-) mice. These studies, together with our previous studies, demonstrate that MIP-1alpha plays a role in both the afferent (T(1)/T(2) development) and efferent (T(1)-mediated leukocyte recruitment) phases of cell-mediated immunity to C. neoformans.
机译：巨噬细胞炎性蛋白1alpha（MIP-1alpha / CCL3）是一种CC趋化因子，是针对隐球菌Ags最佳募集白细胞所必需的。 MIP-1alpha在新隐球菌感染后第6天在肺中表达，并可能在细胞介导的免疫反应中发挥作用。为了解决这种可能性，野生型（MIP-1alpha（+ / +））小鼠和MIP-1alpha敲除（MIP-1alpha（-/-））小鼠在气管内感染了高毒力的新孢梭菌（145A） 。在第3、7和14天，在MIP-1alpha（+ / +）小鼠的肺中检测到MIP-1alpha消息，但在MIP-1alpha（-/-）小鼠中未检测到。在第16天，MIP-1alpha（-/-）小鼠的肺部新孢子虫负担增加了7倍，但肺白细胞募集却没有减少。 MIP-1alpha（+ / +）和MIP-1alpha（-/-）小鼠的募集淋巴细胞和单核细胞/巨噬细胞的数量相似。值得注意的是，MIP-1alpha（-/-）小鼠的嗜酸性粒细胞数量明显增加。 MIP-1alpha（-/-）小鼠的血清IgE水平极高。与MIP-1alpha（+ / +）小鼠相比，MIP-1alpha（-/-）小鼠肺部这种免疫应答转换为T（2）表型与增强的IL-4和IL-13表达相关。在非保护性T（2）免疫存在下肺隐球菌病的进展导致MIP-1alpha（-/-）小鼠受到严重的肺损伤（嗜酸性晶体沉积，肺实质破坏和肺出血）。 MIP-1alpha（-/-）小鼠的十二周生存期显着降低。这些研究以及我们以前的研究表明，MIP-1alpha在细胞介导的传入（T（1）/ T（2）发育）和传出（T（1）介导的白细胞募集）阶段均起作用对新孢子虫的免疫力。

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