https://scholars.lib.ntu.edu.tw/handle/123456789/502804
標題: | Enterovirus 71 infection shapes host T cell receptor repertoire and presumably expands VP1-specific TCRβ CDR3 cluster | 作者: | Liao Y.-W. Ho B.-C. Chen M.-H. SUNG-LIANG YU |
關鍵字: | CDR3; Enterovirus 71; Pathogenesis; TCRβ repertoires; VP1 | 公開日期: | 2020 | 卷: | 9 | 期: | 2 | 來源出版物: | Pathogens | 摘要: | Enterovirus 71 (EV71) has become an important public health problem in the Asia-Pacific region in the past decades. EV71 infection might cause neurological and psychiatric complications and even death. Although an EV71 vaccine has been currently approved, there is no effective therapy for treating EV71-infected patients. Virus infections have been reported to shape host T cell receptor (TCR) repertoire. Therefore, understanding of host TCR repertoire in EV71 infection could better the knowledge in viral pathogenesis and further benefit the anti-viral therapy development. In this study, we used a mouse-adapted EV71 (mEV71) model to observe changes of host TCR repertoire in an EV71-infected central nervous system. Neonate mice were infected with mEV71 and mouse brainstem TCRβ repertoires were explored. Here, we reported that mEV71 infection impacted host brainstem TCRβ repertoire, where mEV71 infection skewed TCRβ diversity, changed VJ combination usages, and further expanded specific TCRβ CDR3 clones. Using bioinformatics analysis and ligand-binding prediction, we speculated the expanded TCRβ CDR3 clone harboring CASSLGANSDYTF sequence was capable of binding cleaved EV71 VP1 peptides in concert with major histocompatibility complex (MHC) molecules. We observed that mEV71 infection shaped host TCRβ repertoire and presumably expanded VP1-specific TCRβ CDR3 in mEV71-infected mouse brainstem that integrated EV71 pathogenesis in central nervous system. ? 2020 by the authors. Licensee MDPI, Basel, Switzerland. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/502804 | ISSN: | 2076-0817 | DOI: | 10.3390/pathogens9020121 | SDG/關鍵字: | complement receptor; protein CDR3; protein VP1; T lymphocyte receptor; T lymphocyte receptor beta chain; unclassified drug; animal experiment; animal model; Article; binding affinity; bioinformatics; cell expansion; central nervous system; central nervous system infection; controlled study; Enterovirus A71; Enterovirus infection; ligand binding; major histocompatibility complex; molecular cloning; mouse; mouse model; nonhuman; pathogenesis; prediction; protein cleavage; protein protein interaction; VDJ recombination |
顯示於: | 醫學檢驗暨生物技術學系 |
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