Ignet

Gene Information

Gene symbol: CD69

Gene name: CD69 molecule

HGNC ID: 1694

Synonyms: CLEC2C

Related Genes

#	Gene Symbol	Number of hits
1	BTLA	1 hits
2	CCL4	1 hits
3	CD4	1 hits
4	CD8A	1 hits
5	CDC42	1 hits
6	CSF2	1 hits
7	CXCL1	1 hits
8	CXCL10	1 hits
9	CXCR5	1 hits
10	DDX58	1 hits
11	EGR1	1 hits
12	FASLG	1 hits
13	GZMB	1 hits
14	IFNG	1 hits
15	IL17A	1 hits
16	IL2	1 hits
17	IL2RA	1 hits
18	IL8	1 hits
19	LAMP1	1 hits
20	MAPK1	1 hits
21	NFKBID	1 hits
22	NR4A2	1 hits
23	PDCD1	1 hits
24	PTGS2	1 hits
25	SLC7A5	1 hits
26	TNFSF10	1 hits
27	XCL1	1 hits

Related Sentences

#	PMID	Sentence
1	28932637	The results further demonstrate that targeting MUC1-C results in enhanced effector function of CD8+ tumor-infiltrating lymphocytes (TILs) as evidenced by increased expression of the activation marker CD69, the degranulation marker CD107α, and granzyme B.
2	28932637	Analysis of gene expression data sets further showed that overexpression of MUC1 in NSCLCs correlates negatively with CD8, IFNG and GZMB, and that decreases in CD8 and IFNG are associated with poor clinical outcomes.
3	28248972	Novel CD28 antagonist mPEG PV1-Fab' mitigates experimental autoimmune uveitis by suppressing CD4+ T lymphocyte activation and IFN-γ production.
4	28248972	A decrease in the activation profile of both T CD4+ and T CD8+ eye-infiltrating lymphocytes was evidenced.
5	28248972	In the periphery, T CD4+ cells from PV1-treated mice also showed a decrease in their activation status, with reduced expression of CD69, CD25, and PD-1 molecules.
6	28248972	In addition, frequency of CD4+IFN-γ+ T cells was significantly lower in PV1-treated group, but not of IL-17-producing T cells.
7	28248972	Moreover, after specific restimulation, PV1 blockade selectively blocked IFN-γ production by CD4+ lymphocytes Taken together, our data suggest that mPEG PV1-Fab' acts mainly on IFN-γ-producing CD4+ T cells and emphasize that this specific CD28 blockade strategy is a potential specific and alternative tool for the treatment of autoimmune disorders in the eye.
8	28186087	These antitumor effects were CD8⁺ T-cell and NK cell dependent; however, they were found to be CD4⁺ T-cell independent.
9	28186087	We found that BV directly stimulated NK cells, induced the expression of the activation marker CD69 and promoted interferon-gamma (IFN-γ) production and cytotoxicity.
10	27531854	These cells were the major source of IL21 in tumors and represented about 10% of the CD4⁺ T-cell population at levels comparable with the T_FH cells present in lymph nodes.
11	27531854	However, these T_FH-like cells displayed a unique CXCR5^-PD-1^lo/-BTLA^-CD69^hi tissue-resident phenotype with substantial IFNγ production, which differed from the phenotype of T_FH cells.
12	27531854	Toll-like receptor 4 (TLR4)-elicited innate monocyte inflammation was important for IL21⁺ T_FH-like cell induction in tumors, and activation of STAT1 and STAT3 was critical for T_FH-like cell polarization in this process.
13	26690514	Expression of EGR1/2/3, IL8, CXCL1, PTGS2, CD69, IFNG, FASLG, CCL4, CDC42, DDX58, NFKBID and NR4A2 genes were independently validated; EGR1/2/3 and IL8 showed >8-fold higher expression in cases relative to the controls implying their important role in CAD.
14	26582197	CD4(+) T-cells in systemic lupus erythematosus (SLE) patients show altered T-cell receptor signaling, which utilizes Fc-receptor γ-chain FcRγ-Syk.
15	26582197	In this study, we show that the ICs present in SLE patients by ligating to FcγRIIIa on CD4(+) T-cells phosphorylate Syk and provide a co-stimulatory signal to CD4(+) T-cells in the absence of CD28 signal.
16	26582197	This led to the development of pathogenic IL-17A(+) and IFN-γ(high) CD4(+) T-cells in vitro.
17	26582197	Cytokines IL-1β, IL-6, TGF-β1, and IL-23 were the only requirement for the development of both populations.
18	26582197	SLE patients CD4(+) T-cells that expressed CD25, CD69, and CD98 bound to ICs showed pSyk and produced IFN-γ and IL-17A.
19	26582197	FcγRIIIa-pSyk up-regulated several toll-like receptor genes as well as the HMGB1 and MyD88 gene transcripts.
20	26320191	NK cell priming with activated pDCs resulted in TRAIL and CD69 up-regulation on NK cells and IFN-γ production.
21	24725595	Accordingly, transfection of miR-27 into human T cells attenuates TCR-induced activation of mitogen-activated protein kinases (MAPKs) and induction of CD69.
22	24055089	Statistical analysis indicated 6 genes, namely IFNG, IL2, XCL1, CD69, CSF2 and CXCL10, as significantly upregulated by PTx which was also demonstrated at the protein level for genes encoding secreted proteins.
23	23847096	Interestingly, submicromolar doses of iPA stimulate resting human NK cells and synergize with IL-2 to induce a robust activation ex vivo with significant secretion of CCL5 and CCL3 and a large increase in TNF-α and IFN-γ production when compared with IL-2 single cytokine treatment.
24	23847096	Moreover, iPA promotes NK cell proliferation and up-regulates the expression of specific NK cell-activating receptors, as well as CD69 and CD107a expression.
25	23668260	The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection.
26	23668260	However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25.
27	23668260	Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc.
28	23668260	They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling.
29	23668260	These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.