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ES-62未能抑制对其他丝虫线虫抗原的1型辅助性T细胞应答。

Failure of ES-62 to inhibit T-helper type 1 responses to other filarial nematode antigens.

作者信息

Al-Riyami L, Egan C A, Bradley J E, Lustigman S, Harnett W

机构信息

Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 27 Taylor Street, Glasgow G4 0NR, UK.

出版信息

Parasite Immunol. 2008 May;30(5):304-8. doi: 10.1111/j.1365-3024.2008.01024.x. Epub 2008 Feb 27.

Abstract

ES-62 is a secreted protein of filarial nematodes that possesses multiple immunomodulatory activities. A full characterization of these activities awaits elucidation but to date it has been shown that ES-62 can inhibit pro-inflammatory/Th1 immune responses and in some studies, it has been found to actively support Th2 development. As an active filarial nematode infection is associated with a Th2-like immunological phenotype, this study investigated whether ES-62 was likely to be responsible for, or at least contribute to, this phenotype. Specifically, we determined ES-62's effect on the immune response to two other filarial nematode antigens, chosen for their ability to promote Th1 responses. The two antigens were recombinant Onchocerca volvulus-Fatty acid And Retinol-binding-1 (rOv-FAR-1) and recombinant Onchocerca volvulus-Activation associated Secreted Protein-1 (Ov-ASP-1). Overall the results show that in spite of its previously characterized immunomodulatory properties, ES-62 was unable to modulate/reverse the Th1 immune responses induced by the two Onchocerca antigens. Therefore, in this study no support is provided for the idea that ES-62 might be a major player in facilitating the overall immunological phenotype in filariasis and reasons for this somewhat surprising outcome are discussed.

摘要

ES-62是一种丝状线虫分泌蛋白,具有多种免疫调节活性。这些活性的全面特征有待阐明,但迄今为止已表明ES-62可抑制促炎/Th1免疫反应,并且在一些研究中,发现它能积极支持Th2的发育。由于活跃的丝状线虫感染与Th2样免疫表型相关,本研究调查了ES-62是否可能对此表型负责,或至少对此表型有贡献。具体而言,我们确定了ES-62对针对另外两种丝状线虫抗原的免疫反应的影响,选择这两种抗原是因为它们具有促进Th1反应的能力。这两种抗原分别是重组盘尾丝虫脂肪酸和视黄醇结合蛋白-1(rOv-FAR-1)以及重组盘尾丝虫激活相关分泌蛋白-1(Ov-ASP-1)。总体结果表明,尽管ES-62具有先前已表征的免疫调节特性,但它无法调节/逆转由这两种盘尾丝虫抗原诱导的Th1免疫反应。因此,本研究不支持ES-62可能是促进丝虫病整体免疫表型的主要因素这一观点,并讨论了这一有些令人惊讶的结果的原因。

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