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[寄生虫感染中免疫反应的损害]

[Impairment of immune response in parasitic infections].

作者信息

Capron A, Camus D, Dessaint J P, le Boubennec-Fischer E

出版信息

Ann Immunol (Paris). 1977 Jan-Mar;128(1-2):541-56.

PMID:848904
Abstract

Parasite escape mechanisms may depend upon factors intrinsic to parasites (host antigen uptake, antigenic variation) and upon partial failure of host's immune mechanisms. Impairment of immune response in parasitic infections, analysed and discussed from literature (138 references), is characterized by a high prevalence of autoantibodies and the common observation of immunosuppression in human parasitic infections as well as in experimental models. The high prevalence of autoantibodies accompanying increased levels of immunoglobulins contrasts with the low prevalence of autoimmune diseases in parasitic endemic areas. Evidence for cell mediated autoimmune process has rarely been reported. This might be related to an impairment of T-helper cell function and to the direct role, on B cells, of mitogens from parasite origin. Immunosuppression has been described in many human parasitic infections and in numerous experimental models. The defect in host's immune response is expressed by an impairment of both humoral and cell mediated immune responses to various heterologous antigens, and increased susceptibility to tumorigenesis, prolonged survival of skin allografts and an increased susceptibility to bacterial or viral infections. Various mechanisms of immunosuppression have been described, including failure of macrophage function or release of soluble immunosuppressive factors by parasites. The authors report some of their recent experiments in experimental schistosomiasis, which have allowed the characterization of such factors. Parasites appear in general to play a role in the regulation of the immune response that they have themselves evoked.

摘要

寄生虫逃逸机制可能取决于寄生虫自身的因素(宿主抗原摄取、抗原变异)以及宿主免疫机制的部分失效。从文献(138篇参考文献)中分析和讨论的寄生虫感染中免疫反应的损害,其特征是自身抗体的高流行率以及在人类寄生虫感染和实验模型中常见的免疫抑制现象。自身抗体的高流行率伴随着免疫球蛋白水平的升高,这与寄生虫流行地区自身免疫性疾病的低流行率形成对比。细胞介导的自身免疫过程的证据很少被报道。这可能与辅助性T细胞功能的损害以及寄生虫来源的丝裂原对B细胞的直接作用有关。免疫抑制已在许多人类寄生虫感染和众多实验模型中被描述。宿主免疫反应的缺陷表现为对各种异源抗原的体液免疫和细胞介导免疫反应的损害,以及对肿瘤发生的易感性增加、皮肤同种异体移植存活时间延长和对细菌或病毒感染的易感性增加。已经描述了多种免疫抑制机制,包括巨噬细胞功能的失败或寄生虫释放可溶性免疫抑制因子。作者报告了他们最近在实验性血吸虫病中的一些实验,这些实验使得能够对这些因素进行表征。寄生虫总体上似乎在调节它们自身引发的免疫反应中发挥作用。

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