scholarly journals Glucocorticoid‐Induced Tumor Necrosis Factor Receptor Family–Related Protein Triggering Enhances HIV‐Specific CD4+T Cell Cytokine Secretion and Protects HIV‐Specific CD4+T Cells from Apoptosis

2007 ◽  
Vol 196 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Timothy P. Lahey ◽  
Suzanne D. Loisel ◽  
Wendy Wieland‐Alter
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cytokine Secretion ◽  
Cd4 T Cell ◽  
Related Protein ◽  
Necrosis Factor ◽  
Receptor Family

scholarly journals Glucocorticoid-Induced Tumor Necrosis Factor Receptor Family-Related Protein Regulates CD4+T Cell–Mediated Colitis in Mice

2012 ◽  
Vol 142 (3) ◽  
pp. 582-591.e8 ◽  
Author(s):  
Gongxian Liao ◽  
Cynthia Detre ◽  
Scott B. Berger ◽  
Pablo Engel ◽  
Rene de Waal Malefyt ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cd4 T Cell ◽  
Related Protein ◽  
Necrosis Factor ◽  
Receptor Family

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 TRANCE Is a Novel Ligand of the Tumor Necrosis Factor Receptor Family That Activates c-Jun N-terminal Kinase in T Cells

1997 ◽  
Vol 272 (40) ◽  
pp. 25190-25194 ◽  
Author(s):  
Brian R. Wong ◽  
Jaerang Rho ◽  
Joseph Arron ◽  
Elizabeth Robinson ◽  
Jason Orlinick ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Necrosis Factor ◽  
Receptor Family
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