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Whether and how regulatory T cells (Treg) are involved in this postseptic immunosuppression is unknown. We observed in vivo that early activation of Treg during Staphylococcus aureus sepsis induces CD4+ T-cell impairment and increases susceptibility to secondary pneumonia. The tumor necrosis factor receptor 2 positive (TNFR2pos) Treg subset endorsed the majority of effector immunosuppressive functions, and TNRF2 was particularly associated with activation of genes involved in cell cycle and replication in Treg, probably explaining their maintenance. Blocking or deleting TNFR2 during sepsis decreased the susceptibility to secondary infection. In humans, our data paralleled those in mice; the expression of CTLA-4 was dramatically increased in TNFR2pos Treg after culture in vitro with S. aureus. Our findings describe in vivo mechanisms underlying sepsis-induced immunosuppression and identify TNFR2pos Treg as targets for therapeutic intervention.<\/jats:p>","DOI":"10.1093\/infdis\/jiaa225","type":"journal-article","created":{"date-parts":[[2020,5,2]],"date-time":"2020-05-02T04:08:39Z","timestamp":1588392519000},"page":"1222-1234","source":"Crossref","is-referenced-by-count":18,"title":["Regulatory T Cells Expressing Tumor Necrosis Factor Receptor Type 2 Play a Major Role in CD4+ T-Cell Impairment During Sepsis"],"prefix":"10.1093","volume":"222","author":[{"given":"Benjamin J","family":"Gaborit","sequence":"first","affiliation":[{"name":"EA3826 Th\u00e9rapeutiques Anti-Infectieuses, Institut de Recherche en Sant\u00e9 2 Nantes Biotech, Universit\u00e9 de Nantes, Nantes, France"},{"name":"Department of Infectious Diseases, University Hospital of Nantes, CIC, INSERM, Nantes, 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