Sepsis-induced changes in differentiation, maintenance, and function of memory CD8 T cell subsets

Abstract

Formation of long-lasting memory lymphocytes is one of the foundational characteristics of adaptive immunity and the basis of many vaccination strategies. Following the rapid expansion and contraction of effector CD8 T cells, the surviving antigen (Ag)-specific cells give rise to the memory CD8 T cells that persist for a long time and are phenotypically and functionally distinct from their naïve counterparts. Significant heterogeneity exists within the memory CD8 T cell pool, as different subsets display distinct tissue localization preferences, cytotoxic ability, and proliferative capacity, but all memory CD8 T cells are equipped to mount an enhanced immune response upon Ag re-encounter. Memory CD8 T cells demonstrate numerical stability under homeostatic conditions, but sepsis causes a significant decline in the number of memory CD8 T cells and diminishes their Ag-dependent and -independent functions. Sepsis also rewires the transcriptional profile of memory CD8 T cells, which profoundly impacts memory CD8 T cell differentiation and, ultimately, the protective capacity of memory CD8 T cells upon subsequent stimulation. This review delves into different aspects of memory CD8 T cell subsets as well as the immediate and long-term impact of sepsis on memory CD8 T cell biology.

Broad-Spectrum Clearance of Lipopolysaccharides from Blood Based on a Hemocompatible Dihistidine Polymer

“…Sepsis is a syndrome of systemic inflammatory response due to a dysregulated host response to infection by pathogenic microorganisms, which can induce multiorgan failure and microcirculatory disturbances. , Statistics show that approximately 50 million people suffer from sepsis each year worldwide, with a mortality rate of up to 40–60%. − Sepsis has become one of the critical diseases in intensive care unit with high prevalence, rapid progression, high mortality, and high hospital costs. , The inability to identify the pathogen of infection in a timely manner necessitates the use of broad-spectrum antibiotics as the first line of clinical treatment. However, the outcomes were not favorable as the administration of broad-spectrum antibiotics caused significantly nephrotoxicity and neurotoxicity, and the long-term abuse of broad-spectrum antibiotics can even lead to dysbiosis and increased antibiotic resistance, , which can make sepsis treatment more challenging.…”

Blood immune profiles reveal a CXCR3/CCR5 axis of dysregulation in early sepsis

“…T cells are essential mediators of the host response to sepsis, but recent studies have also indicated that T cell dysregulation impaired this response 39, 40, 41 . This includes all main T cells subtypes from effector CD4 and CD8, regulatory (Treg) and memory T cells 42, 43, 44 . To assess whether significant T cells changes can be detected in blood samples from our sepsis-suspected patients, we performed multiplex flow cytometry analysis using a T cell activation panel (TCAP; Fig.…”

Sublethal whole-body irradiation induces permanent loss and dysfunction in pathogen-specific circulating memory CD8 T cell populations

“…In contrast to WBI, T N and T CIRCM cells both show the same degree of susceptibility to sepsis-induced apoptosis ( 20 , 48 ) and shortly after sepsis, both T N and T CIRCM cells numerically recover. Additionally, the homeostatic cues from the postseptic environment favor the rapid proliferation of T CM cells, leading to an overrepresentation of central memory phenotype ( 21 , 49 ). Of note, WBI induces cell death through irreversible DNA damage, whereas cytokine-mediated apoptosis is responsible for lymphopenia associated with sepsis.…”