ArticleShock (Augusta, Ga.)2015
Full activation of CD4+ T cells early during sepsis requires specific antigen.
Article in Shock (Augusta, Ga.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Extracellular Lipopolysaccharide Triggers the Release of Unconjugated Interferon-Stimulated Gene 15 (ISG15) Protein from Macrophages via Type-I Interferon/Caspase-4/Gasdermin-D Pathway.Pathogens (Basel, Switzerland) · 2026Article
- IL17FMolecular medicine (Cambridge, Mass.) · 2026Article
- Multi-omic analysis of PBMCs in sepsis reveals widespread cytotoxic dysfunction and an increased population ofFrontiers in immunology · 2025Article
- HP promotes neutrophil inflammatory activation by regulating PFKFB2 in the glycolytic metabolism of sepsis.PloS one · 2024Article
- Immunomodulation of endothelial cells induced by macrolide therapy in a model of septic stimulation.Immunity, inflammation and disease · 2021Article
- Inflammation and Cell Death of the Innate and Adaptive Immune System during Sepsis.Biomolecules · 2021Review
- Bone marrow is the preferred site of memory CD4+ T cell proliferation during recovery from sepsis.JCI insight · 2020Article
- Oxidation-Specific Epitopes (OSEs) Dominate the B Cell Response in Murine Polymicrobial Sepsis.Frontiers in immunology · 2020Article
- Antibody Production in Murine Polymicrobial Sepsis-Kinetics and Key Players.Frontiers in immunology · 2020Article
- Immune Response Resetting in Ongoing Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Cold-inducible RNA-binding protein activates splenic T cells during sepsis in a TLR4-dependent manner.Cellular & molecular immunology · 2018Article
- Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.PloS one · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During sepsis, CD4 T cells express activation markers within the first 24 h. In the present study, the mechanisms of T-cell activation and its consequences were addressed in an acute peritonitis model in mice. The response of CD4+ T cells to sepsis induction was compared between OTII mice, characterized by ovalbumin-specific T-cell receptor-transgenic T cells, and C57BL/6 controls (wild type [WT] mice). Because ovalbumin was absent during peritonitis, the OTII CD4+ T cells could not be activated by canonical antigen recognition. In both OTII and WT control mice, CD4+ T effector cells and CD4+ Foxp3+ regulatory T cells (Tregs) expressed the activation marker CD69 early after sepsis onset. However, full activation with upregulation of CD25 and proliferation took place only in the presence of the antigen. Besides this, the fraction of Tregs was lower in OTII than that in WT mice. Sepsis mortality was increased in OTII mice. Our data show that, in sepsis, partial activation of CD4+ T cells is induced by a T-cell receptor-independent pathway, whereas full stimulation and proliferation require a specific antigen. Antigen-dependent T-cell effector functions as well as Treg activity may contribute to sepsis survival.
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