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首页> 外文期刊>Microbes and infection >TNF but not Fas ligand provides protective anti-L-major immunity in C57BL/6 mice
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TNF but not Fas ligand provides protective anti-L-major immunity in C57BL/6 mice

机译：TNF而非Fas配体在C57BL / 6小鼠中提供保护性的抗L大免疫力

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摘要

The pro-inflammatory cytokine TNF is essential for a protective immune response to some but not all strains of Leishmania major. TNF-deficient mice of a resistant genetic background succumbed rapidly to an infection with L. major BNI. Another member of the TNF superfamily, Fas ligand (FasL), has also been reported to be critical for the immune response to L. major. To test the relative importance of TNF versus FasL for the control of L. major BNI, we infected wildtype C57BL/6 (M.WT), B6.TNF-/-, B6.gld and C57BL/6.gld x TNF-/- (B6.gld.TNF-/-) double-negative mice. Visceral, fatal disease was only observed in B6.TNF-/- mice. but not in 136 gld mice. The course of infection and the immune response of B6.gld.TNF-/- mice were similar to those of B6.TNF-/- mice. B6.gld.TNF-/- juice had a high tissue parasite burden and expressed prominent amounts of inducible nitric oxide synthase (iNOS) in the skin, the lymph nodes (LN) and the spleen as previously reported for B6.TNF-/- mice, whereas the tissue parasite load and the iNOS expression of B6.gld mice resembled that of B6.WT controls. Neither the TNF- nor the FasL-deficiency exerted a detectable intrinsic effect on the proliferation of T cells. Thus, TNF, but not FasL is essential for the control of L. major BNl. The discrepancy between these and other published data are most likely due to the use of different strains of the pathogen. (C) 2005 Elsevier SAS. All rights reserved.
机译：促炎性细胞因子TNF是对部分但不是全部利什曼原虫菌株的保护性免疫应答所必需的。具有抗性遗传背景的TNF缺陷型小鼠迅速死于L. major BNI感染。 TNF超家族的另一个成员Fas配体（FasL）也据报道对于大肠埃希氏菌的免疫反应至关重要。为了测试TNF与FasL在控制大型BNI中的相对重要性，我们感染了野生型C57BL / 6（M.WT），B6.TNF-/-，B6.gld和C57BL / 6.gld x TNF- / -（B6.gld.TNF-/-）双阴性小鼠。内脏致死性疾病仅在B6.TNF-/-小鼠中观察到。但不是136只gld小鼠。 B6.gld.TNF-/-小鼠的感染过程和免疫应答与B6.TNF-/-小鼠相似。 B6.gld.TNF-/-汁液具有较高的组织寄生虫负担，并且在皮肤，淋巴结（LN）和脾脏中表达了大量的诱导型一氧化氮合酶（iNOS），如先前针对B6.TNF-/-的报道。小鼠，而B6.gld小鼠的组织寄生虫负荷和iNOS表达与B6.WT对照相似。 TNF缺陷和FasL缺陷均未对T细胞的增殖产生可检测的内在作用。因此，TNF，而不是FasL对于控制大乳杆菌BN1是必不可少的。这些和其他已发布数据之间的差异很可能是由于使用了不同的病原体菌株造成的。 （C）2005 Elsevier SAS。版权所有。

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