Potential contribution of increased soluble IL-2R to lymphopenia in COVID-19 patients
Yaguang Zhang, Xiaojing Wang, Xuezhen Li, Dong Xi, Ruizhi Mao, Xiaohui Wu, Shipeng Cheng, Xiaoyu Sun, Chunyan Yi, Zhiyang Ling, Liyan Ma, Qin Ning, Yiru Fang, Bing Sun & Di Wu
Cellular & Molecular Immunology (2020)
Since the outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), more than 6 million cases are confirmed and over 300,000 cases are dead after infection. Dysfunction of immunity in COVID-19 patients has been considered as one of the fatal factors for patients, especially cytokine release syndrome and lymphopenia.1,2,3 The reduced number and increased exhaustion level of lymphocyte are associated with elevated inflammatory cytokines in COVID-19 patients.4,5 However, the mechanism of cytokine-induced lymphopenia in COVID-19 is very unclear. IL-2 is critical for the proliferation, differentiation, and function of T cells, including Tregs, CD4+, and CD8+ effector cells.6 Here, we reported the negative relationship between the concentration of soluble IL-2 receptor (sIL-2R) and T-cell number in blood from COVID-19 patients. In vitro addition of recombinant CD25 could inhibit the proliferation and function of T cells from PBMC after stimulated with TCR signaling, which could be rescued by strong IL-2 signaling. Our data suggested the importance of IL-2 signaling in lymphopenia of COVID-19 patients.