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针对布氏锥虫可变表面抗原的体液免疫反应是由退化的寄生虫诱导产生的。

Humoral responses against Trypanosoma brucei variable surface antigen are induced by degenerating parasites.

作者信息

Sendashonga C N, Black S J

出版信息

Parasite Immunol. 1982 Jul;4(4):245-57. doi: 10.1111/j.1365-3024.1982.tb00436.x.

Abstract

An analysis was made of the inductive stimuli for anti-T. brucei variant surface glycoprotein (VSG) responses and the role played by humoral immunity in trypanosome wave control. The first wave parasitaemia was influenced by the rate of parasite differentiation from rapidly dividing slender forms to short lived stumpy forms. Remission of first wave parasitaemia was caused by a humoral immune response against external determinants of surface expressed VSG. Anti-VSG responses were accompanied by anti-trypanosome plasma membrane responses and were followed by non-specific responses. Responses appeared to be initiated by fragments of parasites on which VSG external determinants and plasma membrane antigens were accessible and were possibly accelerated and amplified by a trypanosome mitogen which was not VSG. The parasite fragments may have arisen as a result of degeneration of stumpy form but not slender form parasites.

摘要

对诱导抗布氏锥虫变异表面糖蛋白(VSG)反应的刺激因素以及体液免疫在锥虫血症波控制中所起的作用进行了分析。第一波寄生虫血症受寄生虫从快速分裂的细长型向寿命较短的粗短型分化速率的影响。第一波寄生虫血症的缓解是由针对表面表达的VSG外部决定簇的体液免疫反应引起的。抗VSG反应伴随着抗锥虫质膜反应,随后是非特异性反应。反应似乎由VSG外部决定簇和质膜抗原可及的寄生虫片段引发,并且可能由一种非VSG的锥虫有丝分裂原加速和放大。寄生虫片段可能是粗短型而非细长型寄生虫退化的结果。

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