Ignet

Gene Pair Information

Gene Pair: CD28, IFNG

Related Sentences

#	PMID	Sentence
1	12517723	A reduced capacity to produce this cytokine in the elderly, as demonstrated by our findings of significant decreases in IFN-gamma production in vitro on stimulation with bacterial products (LPS) or viral antigens (influenza vaccine), might therefore contribute to disease susceptibility.
2	12517723	Using tetramer technology and IFN-gamma ELISPOT assays, we found that the commonly-observed clonal expansions of CD8+ T-cells in the elderly were for the most part poorly-functional CMV- and EBV-specific cells, expressing little CD28.
3	20421878	PHF11 is a transcriptional co-activator of the Th1 effector cytokine genes, interleukin-2 (IL2) and interferon-γ (IFNG), co-operating with nuclear factor kappa B (NF-κB).
4	20421878	Consistent with its presence in the nucleus, PHF11 was recruited to the IFNG promoter and over-expression of PHF11 increased the binding of NF-κB to the IFNG promoter and IFNG gene transcription.
5	20421878	Over-expression of PHF11 did not increase IL2 gene transcription, suggesting some specificity in promoter recognition.
6	20421878	In contrast, small-interfering RNA knock-down of PHF11 decreased transcription of both IFNG and IL2 and led to decreased CD28 cell-surface expression and reduced NF-κB nuclear import and DNA binding.
7	20421878	Knock-down of PHF11 also decreased cell viability and was accompanied by reduced expression of GIMAP4 and 5 genes required for T-cell differentiation, viability and homeostasis.
8	21480212	Rapamycin-sensitive signals control TCR/CD28-driven Ifng, Il4 and Foxp3 transcription and promoter region methylation.
9	21480212	Here, we report that both mTOR complex 1 and mTOR complex 2 are readily activated following TCR/CD28 engagement and are critical for early expression of Ifng, Il4 and Foxp3, and for effector T cell differentiation in the absence of polarizing cytokines.
10	21480212	While inhibition of mTOR complex 1 and cell division were evident at low doses of RAPA, inhibition of mTOR complex 2, Ifng, Il4 and Foxp3 expression, and T-cell polarization required higher doses and more prolonged treatments.
11	21480212	We found that while T-bet and GATA3 were readily induced following TCR/CD28 engagement, administration of RAPA delayed their expression, and interfered with the loss of DNA methylation within Ifng and Il4 promoter regions.
12	24313359	Peripheral and site-specific CD4(+) CD28(null) T cells from rheumatoid arthritis patients show distinct characteristics.
13	24313359	Proinflammatory CD4(+) CD28(null) T cells are frequently found in the circulation of patients with rheumatoid arthritis (RA), but are less common in the rheumatic joint.
14	24313359	In the present study, we sought to identify functional differences between CD4(+) CD28(null) T cells from blood and synovial fluid in comparison with conventional CD28-expressing CD4(+) T cells.
15	24313359	Forty-four patients with RA, displaying a distinct CD4(+) CD28(null) T cell population in blood, were recruited for this study; the methylation status of the IFNG locus was examined in isolated T cell subsets, and intracellular cytokine production (IFN-γ, TNF, IL-17) and chemokine receptor expression (CXCR3, CCR6 and CCR7) were assessed by flow cytometry on T cells from the two compartments.
16	24313359	Circulating CD4(+) CD28(null) T cells were significantly more hypomethylated in the CNS-1 region of the IFNG locus than conventional CD4(+) CD28(+) T cells and produced higher levels of both IFN-γ and TNF after TCR cross-linking.
17	24313359	CD4(+) CD28(null) T cells from the site of inflammation expressed significantly more CXCR3 and CCR6 compared to their counterparts in blood.
18	24313359	While IL-17A production could hardly be detected in CD4(+) CD28(null) cells from the blood, a significant production was observed in CD4(+) CD28(null) T cells from synovial fluid.
19	24313359	CD4(+) CD28(null) T cells were not only found to differ from conventional CD4(+) CD28(+) T cells in the circulation, but we could also demonstrate that synovial CD4(+) CD28(null) T cells showed additional effector functions (IL-17 coproduction) as compared to the same subset in peripheral blood, suggesting an active role for these cells in the perpetuation of inflammation in the subset of patients having a CD28(null) population.