Cutting Edge: IL-2 Is Critically Required for the In Vitro Activation of CD4+CD25+ T Cell Suppressor Function

By A. Thornton, Erin Donovan, C. Piccirillo, E. Shevach. Journal of Immunology, 2004

656 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/cb50d5f5d36c3d5bb105d37110e220000c300cc4

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In Immunology

1. Shimon Sakaguchi
2. S. Rosenberg
3. N. Restifo
4. D. Munn
5. A. Mellor
6. P. Krammer
7. Angelika Schmidt
8. Nina Oberle

Citations in the corpus

• Interleukin-2 Receptor Signaling: At the Interface between Tolerance and Immunity (2010, neutral): “, blockade of IL-2 secretion by activated T cells (Thornton et al., 2004).”
• Cytokines in Cancer Immunotherapy (2011, background): “autoimmune colitis [74,76-78], providing additional evidence of the role of IL-2 not only as an activator of immune responses but also as a key mediator of immune tolerance.”
• IL-2 Is Essential for TGF-β to Convert Naive CD4+CD25− Cells to CD25+Foxp3+ Regulatory T Cells and for Expansion of These Cells1 (2007, background): “functional properties of natural CD4 CD25 Treg cells (34, 35).”
• Molecular Mechanisms of Treg-Mediated T Cell Suppression (2012, background): “To be suppressive, Tregs themselves have to be TCR-activated in the presence of IL-2 (Takahashi et al., 1998; Thornton and Shevach, 1998; de la Rosa et al., 2004; Thornton et al., 2004a,b) while costimulation via CD28 is dispensable (Takahashi et al., 2000).”
• Foxp3+CD25+CD4+ natural regulatory T cells in dominant self‐tolerance and autoimmune disease (2006, background): “Exogenous IL-2 may therefore lead to augmentation of Treg-mediated suppression in vivo and in vitro even if it does not exert a significant effect in short-term suppression assays in vitro (55).”
• Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes directly activate mature Tregs via indoleamine 2,3-dioxygenase. (2007, background): “Cocultures were set up as shown in the diagram in Figure 6A and were comprised of IDO+ pDCs, OT-I, feeder cells, mature Tregs (Thy1.”
• TLR Signaling in the Gut in Health and Disease1 (2005, background): “Patients homozygous for the 3020insC frameshift mutation in the Nod2 gene demonstrate defective release of IL-10 from PBMC after stimulation with TLR2 ligands (87).”