The IL-27 receptor regulates TIGIT on memory CD4+ T cells during sepsis
Kristen N. Morrow,
Zhe Liang,
Ming Xue,
Deena B. Chihade,
Yini Sun,
Ching-wen Chen,
Craig M. Coopersmith,
Mandy L. Ford
Affiliations
Kristen N. Morrow
Immunology and Molecular Pathogenesis Program, Laney Graduate School, Emory University, Atlanta, GA 30324, USA; Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA
Zhe Liang
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA
Ming Xue
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA; Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, China
Deena B. Chihade
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA
Yini Sun
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA; Department of Critical Care Medicine, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang 110000, China
Ching-wen Chen
Immunology and Molecular Pathogenesis Program, Laney Graduate School, Emory University, Atlanta, GA 30324, USA; Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA
Craig M. Coopersmith
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA; Emory Critical Care Center, Emory University School of Medicine, Atlanta, GA 30324, USA; Corresponding author
Mandy L. Ford
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30324, USA; Emory Transplant Center, Emory University School of Medicine, Atlanta, GA 30324, USA; Corresponding author
Summary: 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.