Data underlying the research on Molecular mechanism of Cysticercus cellulosae TPx protein regulating Th1/Th2 cell differentiation through JAK/STAT signaling pathway

Cysticercosis is a serious zoonotic parasitic disease caused by the larva of <em>Taenia solium</em> (<em>T. solium</em>), Cysticercus cellulosae, infecting humans or pigs. Currently, the immunopathogenic mechanism of this disease remains unclear. In this study, based on the fact that the thioredoxin peroxidase (TPx) protein in the excretory-secretory antigens (ESA) of Cysticercus cellulosae can induce immune dysfunction of T cells in piglets and produce a Th2-type immune response.Further research was conducted on the effects of TPx protein on the differentiation of human Jurkat T lymphocytes into T helper cell 1 (Th1) and Th2 cells and the changes in the expression levels of proteins related to the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. The results of flow cytometry showed that the TPx protein could promote the differentiation of Th1 cells when acting on human Jurkat T lymphocytes for 24 hours and promote the differentiation of Th2 cells when acting for 48 hours. Transcriptomics and Western blot showed that the TPx protein could activate the JAK/STAT signaling pathway in Jurkat cells. At 48 hours, it upregulated the Th2 cell transcription factor GATA binding protein 3(GATA3) through p-JAK3 and p-STAT6, promoting the differentiation of Th2 cells. This suggests that the JAK/STAT signaling pathway may be an important molecular mechanism for the regulation of Th1/Th2 cell differentiation in Jurkat cells by the TPx protein of Cysticercus cellulosae, providing important scientific evidence for the preliminary revelation of the immunopathogenic mechanism of cysticercosis and the development of vaccines.

囊尾蚴病（Cysticercosis）是由猪带绦虫（Taenia solium，简称T. solium）的幼虫——猪囊尾蚴（Cysticercus cellulosae）感染人类或猪只所引发的严重人畜共患寄生虫病。目前，该病的免疫致病机制仍未明确。本研究基于猪囊尾蚴排泄分泌抗原（ESA）中的硫氧还蛋白过氧化物酶（thioredoxin peroxidase，TPx）可诱导仔猪T细胞免疫功能紊乱并产生Th2型免疫应答这一基础，进一步探究了TPx蛋白对人Jurkat T淋巴细胞向辅助性T细胞1（Th1）与辅助性T细胞2（Th2）分化的影响，以及贾纳斯激酶/信号转导与转录激活因子（Janus kinase/signal transducer and activator of transcription，JAK/STAT）信号通路相关蛋白的表达变化。流式细胞术结果显示，TPx蛋白作用于人Jurkat T淋巴细胞24小时时可促进Th1细胞分化，作用48小时则可推动Th2细胞分化。转录组学（transcriptomics）与蛋白质印迹（Western blot）实验结果表明，TPx蛋白可激活Jurkat细胞内的JAK/STAT信号通路：在干预48小时后，其通过磷酸化JAK3（p-JAK3）与磷酸化STAT6（p-STAT6）上调Th2细胞转录因子GATA结合蛋白3（GATA3）的表达水平，进而促进Th2细胞分化。上述研究结果提示，JAK/STAT信号通路可能是猪囊尾蚴TPx蛋白调控Jurkat细胞Th1/Th2细胞分化的关键分子机制，为初步阐明囊尾蚴病的免疫致病机制及疫苗开发提供了重要科学依据。