CD4(+)CD25(+) immunoregulatory T cells: gene expression analysis reveals a functional role for the glucocorticoid-induced TNF receptor.

By R. McHugh, M. Whitters, C. Piccirillo, D. Young, E. Shevach, M. Collins, M. Byrne. Immunity, 2002

1,632 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4941b33c7fffdbf0202753f4b9d405c394a56579

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In Immunology

Citations in the corpus

Antigen-dependent Proliferation of CD4+ CD25+ Regulatory T Cells In Vivo (2003, result): “The KJ CD25 cells expressed higher OX40 and lower IL-7 receptor than the KJ CD25 cells (Fig.”
Antibody distance from the cell membrane regulates antibody effector mechanisms (2017, background): “CD137 is expressed on resting Tregs and is upregulated following activation (63, 64); therefore, it may serve as a useful target for Treg deletion.”
TGF-β1 Plays an Important Role in the Mechanism of CD4+CD25+ Regulatory T Cell Activity in Both Humans and Mice (2004, background): “As reported previously (18), CD4 CD25 T cells contained a substantial subpopulation of CD103 cells, possibly due to autoactivation.”
Mechanisms of immune evasion by tumors. (2006, background): “Other potential Treg markers include the glucocorticoid‐induced TNF receptor (GITR) (McHugh et al., 2002), neuropilin (Bruder et al.”
Developmental Stage, Phenotype, and Migration Distinguish Naive- and Effector/Memory-like CD4+ Regulatory T Cells (2004, background): “However, in vitro studies did not reveal a higher suppressive potential of the L-selectinhigh subset (19).”
Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes directly activate mature Tregs via indoleamine 2,3-dioxygenase. (2007, background): “Tregs isolated from TDLNs in vivo were constitutively activated, displaying spontaneous suppressor activity that was as potent as the highest levels reported for Tregs extensively activated in vitro (15, 16).”
Foxp3+CD25+CD4+ natural regulatory T cells in dominant self‐tolerance and autoimmune disease (2006, background): “In vitro studies showed that cross-linking of GITR by a specific mAb, together with TCR stimulation, abrogated in vitro CD25CD4 Treg-mediated suppression and also triggered the proliferation of Tregs in the presence of IL-2 (86, 88).”