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先天性利什曼病对后代免疫的潜在影响:T 细胞耐受。

T-cell tolerance as a potential effect of congenital leishmaniasis on offspring immunity.

机构信息

Departamento de Infectología e Inmunología, Instituto Nacional de Perinatología, Secretaria de Salud, Mexico City, Mexico.

Escuela Superior de Medicina, Instituto Politécnico Nacional, Mexico City, Mexico.

出版信息

Parasite Immunol. 2019 Mar;41(3):e12540. doi: 10.1111/pim.12540. Epub 2018 Jun 29.

Abstract

Congenital transmission of leishmaniasis is recognized in cases detected by passive surveillance. Most cases are from low-resource countries, limiting the study of several important aspects of this route of infection, including the offspring's immune response. Studies on natural and experimentally infected animals suggest that parasites might be transmitted to the embryo or foetus at any time during pregnancy. As immune system undergoes sequential stages of development, an infection before the time of self-recognition could lead to central tolerance, making an individual specifically tolerant and susceptible to infection. In the alternative scenario, infection after self-recognition would allow the proper development of T-lymphocyte clones in response to Leishmania antigens, providing resistance to the disease. Newborns undergo a transient period of low expression of several immune surface molecules and a naïve adaptive immune response with no memory, which together might contribute to slow elimination of the parasite over several months. This insight is a proposed independent mechanism of the previously proven T-cell exhaustion and must be investigated. Analyses of infected placenta, cord blood and infant immunity are required for a better understanding of immunity in congenital leishmaniasis infection.

摘要

先天性利什曼病的传播是通过被动监测发现的。大多数病例来自资源匮乏的国家,这限制了对这种感染途径的几个重要方面的研究,包括后代的免疫反应。对自然和实验感染动物的研究表明,寄生虫可能在怀孕期间的任何时候传播到胚胎或胎儿。随着免疫系统经历连续的发育阶段,如果在自我识别之前发生感染,可能会导致中枢耐受,使个体对感染具有特异性的耐受性和易感性。在另一种情况下,在自我识别后发生感染将允许针对利什曼原虫抗原产生 T 淋巴细胞克隆的适当发育,从而对疾病产生抵抗力。新生儿经历了一个免疫表面分子表达水平低和适应性免疫反应无记忆的短暂阶段,这可能共同导致寄生虫在几个月内缓慢消除。这种见解是之前证明的 T 细胞耗竭的一个独立机制,必须进行研究。需要对受感染的胎盘、脐带血和婴儿的免疫进行分析,以更好地了解先天性利什曼病感染中的免疫。

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