The IL-27 receptor regulates TIGIT on memory CD4⁺ T cells during sepsis

• Type of Material: Article
• Authors: Kristen N. Morrow, Emory University; Zhe Liang, Emory University; Ming Xue, Emory University; Deena B. Chihade, Emory University; Yini Sun, Emory University; Ching-wen Chen, Emory University; Craig Coopersmith, Emory University; Mandy Ford, Emory University
• Language: English
• Date: 2021-02-19
• Publisher: Elsevier
• Publication Version: Final Published Version
• Copyright Statement: © 2021 The Authors Molecular Biology; Immunology
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.isci.2021.102093
• Title of Journal or Parent Work: iScience
• Volume: 24
• Issue: 2
• Start Page: 102093
• End Page: 102093
• Grant/Funding Information: The study was funded by NIH R01s GM104323 GM095442, GM072808, and AI149724.
• Keywords: Immunology; Molecular Biology
• Research Categories: Health Sciences, Immunology; Biology, Molecular

Abstract

Sepsis is a leading cause of morbidity and mortality associated with significant impairment in memory T cells. These changes include the upregulation of co-inhibitory markers, a decrease in functionality, and an increase in apoptosis. Due to recent studies describing IL-27 regulation of TIGIT and PD-1, we assessed whether IL-27 impacts these co-inhibitory molecules in sepsis. Based on these data, we hypothesized that IL-27 was responsible for T cell dysfunction during sepsis. Using the cecal ligation and puncture (CLP) sepsis model, we found that IL-27Rα was associated with the upregulation of TIGIT on memory CD4+ T cells following CLP. However, IL-27 was not associated with sepsis mortality.