Ignet

Gene Information

Gene symbol: CD27

Gene name: CD27 molecule

HGNC ID: 11922

Synonyms: S152, Tp55

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	CD44	1 hits
3	CD70	1 hits
4	CD8A	1 hits
5	IDDM2	1 hits
6	IL17A	1 hits
7	MS4A1	1 hits
8	TNFRSF4	1 hits

Related Sentences

#	PMID	Sentence
1	9115575	Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis.
2	9115575	However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005).
3	9115575	IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls.
4	9115575	The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls.
5	9115575	Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes.
6	9115575	Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis.
7	9115575	However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005).
8	9115575	IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls.
9	9115575	The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls.
10	9115575	Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes.
11	9115575	Lymphocytes from 77 newly diagnosed IDDM patients, 58 IDDM patients with disease duration > 6 months and 30 non-diabetic controls (including patients with several inflammatory conditions) were analyzed for membrane expression of CD4, CD8, CD45RA, CD45RO and CD27 molecules by FACS analysis.
12	9115575	However, the percentage of CD4+ T cells, and consequently the CD4/CD8 ratio were significantly increased in PBL of recently diagnosed diabetic patients compared to the non-diabetic control group (P < 0.005).
13	9115575	IDDM patients had a lower percentage of resting memory T cells (CD45RO+ CD27+) than the non-diabetic controls.
14	9115575	The proportion of CD45RO+ lymphocytes lacking the CD27 molecule ((re)-activated memory cells) was similar in IDDM patients and non-diabetic controls.
15	9115575	Our findings confirm and extend previous observations that a disturbance in lymphocyte subset distribution is present in patients with IDDM showing an increase in the percentages of circulating CD4 lymphocytes.
16	11266785	The effect of OX40/OX40L and CD27/CD70 pathways on allogeneic islet graft rejection.
17	12624711	Renal tubule apoptosis is induced by the CD27 ligand, Siva, binding to the truncated tail CD27.
18	17163450	CD8+ suppressor-mediated regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65.
19	17163450	It has been well demonstrated that CD4+ CD25+ regulatory T cells play a significant role in controlling the expansion of autoreactive T cells in the periphery.
20	17163450	However, some healthy individuals exhibit measurable responses to self peptide even in the presence of CD4+ CD25+ regulatory cells.
21	17163450	This article describes the regulation of human CD4+ T cell responses to glutamic acid decarboxylase 65 (GAD65), an autoantigen implicated in type-1 diabetes, by autologous CD8+ suppressor T cells.
22	17163450	In cells cultured from healthy individuals, the inclusion of autologous CD8+ T cells at physiological levels resulted in a dramatic decrease in the magnitude of in vitro CD4+ T cell responses to GAD65 peptide.
23	17163450	Cell fractionation studies suggested that CD8+ suppressor T cells originate from the CD45RA+ CD27- population.
24	17163450	The suppression of CD4+ T cell responses to GAD65 in healthy individuals raises the possibility that CD8+ suppressor T cells play an important role in controlling potentially autoreactive T cells in the general population.
25	18172311	We also found that multiple myeloma cells expressing the memory B-cell markers CD20 and CD27 could give rise to clonogenic multiple myeloma growth in vitro and engraft immunodeficient nonobese diabetes/severe combined immunodeficient mice during both primary and secondary transplantation.
26	23626013	We report that γδ TCR(+) cells, including both the CD27(-)CD44(hi) and CD27(+)CD44(lo) subsets, infiltrate islets of prediabetic NOD mice.
27	23626013	Moreover, NOD CD27(-)CD44(hi) and CD27(+)CD44(lo) γδ T cells were preprogrammed to secrete IL-17, or IFN-γ upon activation.
28	23626013	The potent contributions of CD27(-) γδ T cells and IL-17 to islet inflammation and diabetes reported in this study suggest that these mechanisms may also underlie human T1D.
29	23626013	We report that γδ TCR(+) cells, including both the CD27(-)CD44(hi) and CD27(+)CD44(lo) subsets, infiltrate islets of prediabetic NOD mice.
30	23626013	Moreover, NOD CD27(-)CD44(hi) and CD27(+)CD44(lo) γδ T cells were preprogrammed to secrete IL-17, or IFN-γ upon activation.
31	23626013	The potent contributions of CD27(-) γδ T cells and IL-17 to islet inflammation and diabetes reported in this study suggest that these mechanisms may also underlie human T1D.
32	23626013	We report that γδ TCR(+) cells, including both the CD27(-)CD44(hi) and CD27(+)CD44(lo) subsets, infiltrate islets of prediabetic NOD mice.
33	23626013	Moreover, NOD CD27(-)CD44(hi) and CD27(+)CD44(lo) γδ T cells were preprogrammed to secrete IL-17, or IFN-γ upon activation.
34	23626013	The potent contributions of CD27(-) γδ T cells and IL-17 to islet inflammation and diabetes reported in this study suggest that these mechanisms may also underlie human T1D.