Figure 2.
Sepsis and Tregs. Sepsis is a kind of multi-dimensional heterogeneous syndrome, which is not only reflected in the host's demographics, chronic illness, comorbidities, laboratory abnormalities, infections position, patterns of organ dysfunction and severity of illness, and different types of the pathogen but also reflected in the protean host immune responses, where each is not identical. Sepsis influences the heterogeneous characteristics of Tregs from the aspects of percentage (CD4+CD25+/CD4+), absolute number, phenotypes [cytotoxic T lymphocyte antigen (CTLA)-4, CD25, PD-1, CD43, B- and T-lymphocyte attenuator (BTLA), neuropilin (Nrp)-1, G protein-coupled receptor (GPR) 174, lymphocyte activation gene (LAG)-3 and membrane-associated transforming growth factor-β (TGF-βm+), etc.], cytokines and chemokines [IL-10, TGF-β, IL-3, IL-35, and chemokine (C-X-C motif) ligand (CXCL)-4, etc.] secretion, and stability [Foxp3 expression, suppressive function, and methylation status of the foxp3-Tregs-specific demethylated region (TSDR), etc.].
