scholarly journals Asymptomatic Plasmodial Infection Is Associated With Increased Tumor Necrosis Factor Receptor II–Expressing Regulatory T Cells and Suppressed Type 2 Immune Responses

2013 ◽  
Vol 207 (10) ◽  
pp. 1590-1599 ◽  
Author(s):  
Linda J. Wammes ◽  
Aprilianto E. Wiria ◽  
Christa G. Toenhake ◽  
Firdaus Hamid ◽  
Kit Yeng Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Immune Responses ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Plasmodial Infection ◽  
Necrosis Factor

Regulatory T Cells Expressing Tumor Necrosis Factor Receptor Type 2 Play a Major Role in CD4+ T-Cell Impairment During Sepsis

2020 ◽  
Vol 222 (7) ◽  
pp. 1222-1234 ◽  
Author(s):  
Benjamin J Gaborit ◽  
Antoine Roquilly ◽  
Cédric Louvet ◽  
Abderrahmane Sadek ◽  
Benoit Tessoulin ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cd4 T Cell ◽  
Treg Subset ◽  
Necrosis Factor

Abstract Sepsis causes inflammation-induced immunosuppression with lymphopenia and alterations of CD4+ T-cell functions that renders the host prone to secondary infections. 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.

scholarly journals Costimulation via the tumor-necrosis factor receptor superfamily couples TCR signal strength to the thymic differentiation of regulatory T cells

2014 ◽  
Vol 15 (5) ◽  
pp. 473-481 ◽  
Author(s):  
Shawn A Mahmud ◽  
Luke S Manlove ◽  
Heather M Schmitz ◽  
Yan Xing ◽  
Yanyan Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Signal Strength ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor receptor 2-dependent homeostasis of regulatory T cells as a player in TNF-induced experimental metastasis

2013 ◽  
Vol 34 (6) ◽  
pp. 1296-1303 ◽  
Author(s):  
Martin Chopra ◽  
Simone S. Riedel ◽  
Marlene Biehl ◽  
Stefanie Krieger ◽  
Viktoria von Krosigk ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Experimental Metastasis ◽  
Necrosis Factor

Pretransplant Recipient Circulating CD4+CD127lo/− Tumor Necrosis Factor Receptor 2+ Regulatory T Cells

2016 ◽  
Vol 100 (2) ◽  
pp. 314-324 ◽  
Author(s):  
Minh-Tri J. P. Nguyen ◽  
Elise Fryml ◽  
Sossy K. Sahakian ◽  
Shuqing Liu ◽  
Marcelo Cantarovich ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor

scholarly journals TNFR2 pathways are fully active in cancer regulatory T cells

2022 ◽  
Author(s):  
Yuumi Okuzono ◽  
Yo Muraki ◽  
Shuji Sato
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Regulatory T Cells ◽  
Tumor Necrosis ◽  
Interleukin 2 ◽  
Tumor Necrosis Factor Receptor ◽  
Enrichment Analysis ◽  
Pathway Enrichment Analysis ◽  
Signaling Mechanism ◽  
Necrosis Factor

Abstract Tumor necrosis factor receptor 2 (TNFR2), a membrane-bound tumor necrosis factor receptor expressed by regulatory T cells (Tregs), participates in Treg proliferation. Although a specific TNFR2 pathway has been reported, the signaling mechanism has not been completely elucidated. This study sought to clarify TNFR2 signaling in human Tregs using amplicon sequencing and single-cell RNA-sequencing to assess Tregs treated with a TNFR2 agonist antibody. Pathway enrichment analysis based on differentially expressed genes highlighted tumor necrosis factor α signaling via nuclear factor-kappa B, interleukin-2 signal transducer and activator of transcription 5 signaling, interferon-γ response, and cell proliferation-related pathways in Tregs after TNFR2 activation. TNFR2-high Treg-focused analysis found that these pathways were fully activated in cancer Tregs, showing high TNFR2 expression. Collectively, these findings suggest that TNFR2 orchestrates multiple pathways in cancer Tregs, which could help cancer cells escape immune surveillance, making TNFR2 signaling a potential anticancer therapy target.

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