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在小鼠实验性感染结果中对克氏锥虫Tc13抗原引发的免疫反应的评估。

Evaluation of immune responses raised against Tc13 antigens of Trypanosoma cruzi in the outcome of murine experimental infection.

作者信息

García G A, Arnaiz M R, Esteva M I, Laucella S A, Garavaglia P A, Ibarra S E, Ruiz A M

机构信息

Instituto Nacional de Parasitología Dr. Mario Fatala Chaben - ANLIS/Malbrán, Paseo Colón 568 (cp: 1063), Buenos Aires, Argentina.

出版信息

Parasitology. 2008 Mar;135(3):347-57. doi: 10.1017/S0031182007003873. Epub 2007 Nov 9.

Abstract

We have previously reported that genetic immunization with Tc13Tul antigen of Trypanosoma cruzi, the aetiological agent of Chagas' disease, triggers harmful effects and non-protective immune responses. In order to confirm the role of Tc13 antigens during T. cruzi infection, herein we studied the humoral and cellular immune responses to the Tc13Tul molecule and its EPKSA C-terminal portion in BALB/c T. cruzi-infected mice or mice immunized with recombinant Tc13Tul. Analysis of the antibody response showed that B-cell epitopes that stimulate a sustained IgM production along the infection and high levels of IgG in the acute phase are mainly located at the Tc13 N- and C-terminal domains, respectively. DTH assays showed that T-cell epitopes are mainly at the Tc13 N-terminal segment and that they do not elicit an efficient memory response. Recombinant Tc13Tul did not induce IFN-gamma secretion in either infected or immunized mice. However, a putative CD8+Tc13Tul-derived peptide was found to elicit IFN-gamma production in chronically infected animals. Immunization with recombinant Tc13Tul did not induce pathology in tissues and neither did it protect against the infection. Our results show that in the outcome of T. cruzi infection the Tc13 family protein mainly triggers non-protective immune responses.

摘要

我们之前曾报道,用恰加斯病的病原体克氏锥虫的Tc13Tul抗原进行基因免疫会引发有害效应和非保护性免疫反应。为了证实Tc13抗原在克氏锥虫感染过程中的作用,在此我们研究了BALB/c克氏锥虫感染小鼠或用重组Tc13Tul免疫的小鼠对Tc13Tul分子及其EPKSA C末端部分的体液免疫和细胞免疫反应。抗体反应分析表明,在感染过程中刺激持续产生IgM以及在急性期刺激产生高水平IgG的B细胞表位分别主要位于Tc13的N末端和C末端结构域。迟发型超敏反应试验表明,T细胞表位主要位于Tc13的N末端片段且它们不会引发有效的记忆反应。重组Tc13Tul在感染或免疫的小鼠中均未诱导IFN-γ分泌。然而,发现一个推定的源自CD8+Tc13Tul的肽在慢性感染动物中引发IFN-γ产生。用重组Tc13Tul免疫不会诱导组织病变,也不能预防感染。我们的结果表明,在克氏锥虫感染的结果中,Tc13家族蛋白主要引发非保护性免疫反应。

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