ArticleJournal of immunology (Baltimore, Md. : 1950)2023
Inefficient Recovery of Repeatedly Stimulated Memory CD8 T Cells after Polymicrobial Sepsis Induction Leads to Changes in Memory CD8 T Cell Pool Composition.
Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- IL-15/NKG2D signaling-mediated activation of CD8Journal of thoracic disease · 2026Article
- The transcription factor ZNF683 marks an exhaustion-like GZMBFrontiers in immunology · 2026Article
- The Role and Research Progress of CD8Biomedicines · 2025Review
- The ability of memory CD8 T cell subsets to numerically and functionally recover following whole body irradiation is influenced by their history of cognate antigen exposures.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Accurate enumeration of pathogen-specific and virtual memory CD8 T cells after infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- Metabolic reprogramming and dysregulated IL-17 production impairs CD4 T cell function post sepsis.iScience · 2024Article
- Sepsis-induced changes in differentiation, maintenance, and function of memory CD8 T cell subsets.Frontiers in immunology · 2023Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Long-lasting sepsis-induced immunoparalysis has been principally studied in primary (1°) memory CD8 T cells; however, the impact of sepsis on memory CD8 T cells with a history of repeated cognate Ag encounters is largely unknown but important in understanding the role of sepsis in shaping the pre-existing memory CD8 T cell compartment. Higher-order memory CD8 T cells are crucial in providing immunity against common pathogens that reinfect the host or are generated by repeated vaccination. In this study, we analyzed peripheral blood from septic patients and show that memory CD8 T cells with defined Ag specificity for recurring CMV infection proliferate less than bulk populations of central memory CD8 T cells. Using TCR-transgenic T cells to generate 1° and higher-order (quaternary [4°]) memory T cells within the same host, we demonstrate that the susceptibility and loss of both memory subsets are similar after sepsis induction, and sepsis diminished Ag-dependent and -independent (bystander) functions of these memory subsets equally. Both the 1° and 4° memory T cell populations proliferated in a sepsis-induced lymphopenic environment; however, due to the intrinsic differences in baseline proliferative capacity, expression of receptors (e.g., CD127/CD122), and responsiveness to homeostatic cytokines, 1° memory T cells become overrepresented over time in sepsis survivors. Finally, IL-7/anti-IL-7 mAb complex treatment early after sepsis induction preferentially rescued the proliferation and accumulation of 1° memory T cells, whereas recovery of 4° memory T cells was less pronounced. Thus, inefficient recovery of repeatedly stimulated memory cells after polymicrobial sepsis induction leads to changes in memory T cell pool composition, a notion with important implications in devising strategies to recover the number and function of pre-existing memory CD8 T cells in sepsis survivors.
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