title: Impact of sepsis on CD4 T cell immunity.
abstract: Sepsis remains the primary cause of death from infection in hospital patients, despite improvements in antibiotics and intensive-care practices. Patients who survive severe sepsis can display suppressed immune function, often manifested as an increased susceptibility to (and mortality from) nosocomial infections. Not only is there a significant reduction in the number of various immune cell populations during sepsis, but there is also decreased function in the remaining lymphocytes. Within the immune system, CD4 T cells are important players in the proper development of numerous cellular and humoral immune responses. Despite sufficient clinical evidence of CD4 T cell loss in septic patients of all ages, the impact of sepsis on CD4 T cell responses is not well understood. Recent findings suggest that CD4 T cell impairment is a multipronged problem that results from initial sepsis-induced cell loss. However, the subsequent lymphopenia-induced numerical recovery of the CD4 T cell compartment leads to intrinsic alterations in phenotype and effector function, reduced repertoire diversity, changes in the composition of naive antigen-specific CD4 T cell pools, and changes in the representation of different CD4 T cell subpopulations (e.g., increases in Treg frequency). This review focuses on sepsis-induced alterations within the CD4 T cell compartment that influence the ability of the immune system to control secondary heterologous infections. The understanding of how sepsis affects CD4 T cells through their numerical loss and recovery, as well as function, is important in the development of future treatments designed to restore CD4 T cells to their presepsis state.
authors.affiliation: Microbiology, Immunology, and Cancer Biology Graduate Program Medical Scientist Training Program.
authors.forename: Javier
authors.initials: J
authors.lastname: Cabrera-Perez
authors.affiliation: Department of Pathology and.
authors.forename: Stephanie A
authors.initials: SA
authors.lastname: Condotta
authors.affiliation: Department of Pathology and Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
authors.forename: Vladimir P
authors.initials: VP
authors.lastname: Badovinac
authors.affiliation: Microbiology, Immunology, and Cancer Biology Graduate Program Center for Immunology, and Department of Urology, University of Minnesota Medical School, Minneapolis, Minnesota, USA; Minneapolis Veterans Administration Health Care System, Minneapolis, Minnesota, USA; and tgriffit@umn.edu.
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Griffith
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D010641:Phenotype; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines
keywords: apoptosis; homeostatic proliferation; immune suppression; lymphopenia