Ignet

Gene Information

Gene symbol: ICOS

Gene name: inducible T-cell co-stimulator

HGNC ID: 5351

Synonyms: AILIM, CD278

Related Genes

#	Gene Symbol	Number of hits
1	BCL6	1 hits
2	CXCR5	1 hits
3	EGR2	1 hits
4	IFNG	1 hits
5	IL10	1 hits
6	RORC	1 hits
7	TBX21	1 hits
8	TGFB1	1 hits
9	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	28228602	The signature resembled a pre-T helper 1 (T_H1)/T_H17/T follicular helper cell response with expression of CCR6, IL21, TBX21, TNF, RORC, EGR2, TGFB1, and ICOS, in the absence of FOXP3, IL17, and other cytokines.
2	26646149	IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection.
3	26646149	In Plasmodium chabaudi infection, one specific CD4 T cell subset generates anti-parasitic IFN-γ and the antibody-promoting cytokine, IL-21.
4	26646149	While Ifng+ Teff expanded, the level of the Th1 lineage-determining transcription factor T-bet only peaked briefly.
5	26646149	Ifng+ Teff also co-express ICOS, the B cell area homing molecule CXCR5, and other Tfh lineage-associated molecules including Bcl6, the transcription factor required for germinal center (GC) T follicular helper cells (Tfh) differentiation.
6	26646149	Because Bcl6 and T-bet co-localize to the nucleus of Ifng+ Teff, we hypothesized that Bcl6 controls the Tfh-like phenotype of Ifng+ Teff cells in P. chabaudi infection.
7	26646149	Bcl6-deficient T cells did not develop into GC Tfh, but they still generated CXCR5+ IFN-γ+ IL-21+ IL-10+ Teff, suggesting that this predominant population is not of the Tfh-lineage.
8	26646149	IL-10 deficient mice, which have increased IFN-γ and T-bet expression, demonstrated expansion of both IFN-γ+ IL-21+ CXCR5+ cells and IFN-γ+ GC Tfh cells, suggesting a Th1 lineage for the former.
9	26646149	In the memory phase, all Ifng+ T cells produced IL-21, but only a small percentage of highly proliferative Ifng+ T cells maintained a T-bethi phenotype.
10	26253701	CD3⁺ICOS⁺ T cells show differences in the synthesis of nitric oxide, IFN-γ, and IL-10 in patients with pulmonary tuberculosis or in healthy household contacts.
11	26253701	CD3⁺ICOS⁺ T cells show differences in the synthesis of nitric oxide, IFN-γ, and IL-10 in patients with pulmonary tuberculosis or in healthy household contacts.
12	26253701	CD3⁺ICOS⁺ T cells show differences in the synthesis of nitric oxide, IFN-γ, and IL-10 in patients with pulmonary tuberculosis or in healthy household contacts.
13	26253701	CD3⁺ICOS⁺ T cells show differences in the synthesis of nitric oxide, IFN-γ, and IL-10 in patients with pulmonary tuberculosis or in healthy household contacts.
14	26253701	Moreover, T cells synthesise nitric oxide (NO), interferon gamma (IFN-γ), and interleukin (IL)-10, which help regulate the immune response to tuberculosis.
15	26253701	Moreover, T cells synthesise nitric oxide (NO), interferon gamma (IFN-γ), and interleukin (IL)-10, which help regulate the immune response to tuberculosis.
16	26253701	Moreover, T cells synthesise nitric oxide (NO), interferon gamma (IFN-γ), and interleukin (IL)-10, which help regulate the immune response to tuberculosis.
17	26253701	Moreover, T cells synthesise nitric oxide (NO), interferon gamma (IFN-γ), and interleukin (IL)-10, which help regulate the immune response to tuberculosis.
18	26253701	Therefore, we assessed the synthesis of NO, IFN-γ, and IL-10 in CD3⁺ICOS⁺ T cells from healthy individuals, household contacts (HHC), and patients with active pulmonary tuberculosis (PTB), previously stimulated with the antigen H37Rv.
19	26253701	Therefore, we assessed the synthesis of NO, IFN-γ, and IL-10 in CD3⁺ICOS⁺ T cells from healthy individuals, household contacts (HHC), and patients with active pulmonary tuberculosis (PTB), previously stimulated with the antigen H37Rv.
20	26253701	Therefore, we assessed the synthesis of NO, IFN-γ, and IL-10 in CD3⁺ICOS⁺ T cells from healthy individuals, household contacts (HHC), and patients with active pulmonary tuberculosis (PTB), previously stimulated with the antigen H37Rv.
21	26253701	Therefore, we assessed the synthesis of NO, IFN-γ, and IL-10 in CD3⁺ICOS⁺ T cells from healthy individuals, household contacts (HHC), and patients with active pulmonary tuberculosis (PTB), previously stimulated with the antigen H37Rv.
22	26253701	Our results indicated a significant increase in both the percentage of ICOS⁺ cells and CD3⁺ICOS⁺ T cells producing NO, IFN-γ, and IL-10 in cells obtained from patients with PTB (p < 0.01).
23	26253701	Our results indicated a significant increase in both the percentage of ICOS⁺ cells and CD3⁺ICOS⁺ T cells producing NO, IFN-γ, and IL-10 in cells obtained from patients with PTB (p < 0.01).
24	26253701	Our results indicated a significant increase in both the percentage of ICOS⁺ cells and CD3⁺ICOS⁺ T cells producing NO, IFN-γ, and IL-10 in cells obtained from patients with PTB (p < 0.01).
25	26253701	Our results indicated a significant increase in both the percentage of ICOS⁺ cells and CD3⁺ICOS⁺ T cells producing NO, IFN-γ, and IL-10 in cells obtained from patients with PTB (p < 0.01).
26	26253701	In conclusion, results show that the CD3⁺ICOS⁺ T cells obtained from PTB patients are the main producers of NO, IFN-γ, and IL-10.
27	26253701	In conclusion, results show that the CD3⁺ICOS⁺ T cells obtained from PTB patients are the main producers of NO, IFN-γ, and IL-10.
28	26253701	In conclusion, results show that the CD3⁺ICOS⁺ T cells obtained from PTB patients are the main producers of NO, IFN-γ, and IL-10.
29	26253701	In conclusion, results show that the CD3⁺ICOS⁺ T cells obtained from PTB patients are the main producers of NO, IFN-γ, and IL-10.
30	23159227	Unlike ICOS and T-bet deficiency that failed to rescue several autoimmune manifestations, interferon-γ receptor (IFN-γR) deficiency prevented lupus development.