2004
DOI: 10.4049/jimmunol.173.7.4500
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Abstract: CD28 provides important signals that lower the threshold of T cell activation, augment the production of IL-2, and promote T cell survival. The recent identification of a second family of costimulatory molecules within the TNFR family has reshaped the “two-signal” model of T cell activation. In this study the role of p75 as a T cell costimulatory molecule in controlling cell fate during TCR/CD28-mediated stimulation was examined. We found that p75-deficient T cells possess a profound defect in IL-2 production … Show more

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Cited by 90 publications
(93 citation statements)
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References 52 publications
(59 reference statements)
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“…However, there is accumulating evidence that signaling through the TNF-R2 influences a number of pro-inflammatory responses, including the activation of T cells [16][17][18], myofibroblasts [19], inhibition of angiogenesis and tumor suppression [20].…”
Section: A C C E P T E D Article In Pressmentioning
confidence: 99%
“…However, there is accumulating evidence that signaling through the TNF-R2 influences a number of pro-inflammatory responses, including the activation of T cells [16][17][18], myofibroblasts [19], inhibition of angiogenesis and tumor suppression [20].…”
Section: A C C E P T E D Article In Pressmentioning
confidence: 99%
“…The proliferative signals are commonly derived from the activation of p75 TNFR. 12,14,15 To assess the proliferative effect of the secreted mutant mTNF-a in transfected tumor cell culture, we performed the in vitro T-cell proliferation assay. As shown in Figure 1a, the control recombinant TNF-a stimulated CTLL-2T cell proliferation in a dosedependent manner.…”
Section: Resultsmentioning
confidence: 99%
“…[8][9][10] The p55 TNF-a receptor (TNFR) is primarily responsible for signaling in variety of responses including cytotoxicity 11,12 and cytokine secretion, 13 whereas the p75 TNFR is responsible for lymphoproliferative signals and activation of T cells. 12,14,15 To induce high local concentration of TNF-a while limiting systemic use of a high dose of TNF-a, isolated limb perfusion with TNF-a has been applied with less systemic toxicity. 16,17 These results prompted a number of studies aimed at decreasing TNF-a toxicity without modifying its antitumor properties, thereby allowing its use not only for regional treatments but also for systemic therapy.…”
Section: Introductionmentioning
confidence: 99%
“…For example, collecting TNF and ligating it to TNFR1, termed 'ligand passing', 7,11 mediates the anti-tumor effects of TNF when expressed on host innate immune cells, 1 activating different subgroups of T cells during inflammation, tumor growth and autoimmune diseases. [12][13][14][15] Interestingly, TNFR2 expression has also been reported on non-bone marrow (BM)-derived cells, such as vascular endothelial cells. 16 Non-BM TNFR2 expression can function through inhibiting collagen degradation and stimulating the proliferation of intestinal myofibroblasts.…”
Section: Introductionmentioning
confidence: 99%