Ignet

Gene Information

Gene symbol: TREM2

Gene name: triggering receptor expressed on myeloid cells 2

HGNC ID: 17761

Synonyms: TREM-2, Trem2a, Trem2b, Trem2c

Related Genes

#	Gene Symbol	Number of hits
1	APLP2	1 hits
2	BTG1	1 hits
3	CCL2	1 hits
4	CD300LB	1 hits
5	CD4	1 hits
6	CYR61	1 hits
7	EPHA1	1 hits
8	IFNG	1 hits
9	IGFBP3	1 hits
10	IGSF6	1 hits
11	IL8	1 hits
12	KPNA6	1 hits
13	MRPS11	1 hits
14	NCR3	1 hits
15	NFKBIA	1 hits
16	PDCD1LG2	1 hits
17	PGF	1 hits
18	RAD21	1 hits
19	SEMA6A	1 hits
20	SRGN	1 hits
21	TLR4	1 hits
22	TMEM176B	1 hits
23	TNF	1 hits
24	TUBAL3	1 hits
25	TXNRD1	1 hits
26	TYROBP	1 hits

Related Sentences

#	PMID	Sentence
1	19399172	Indirect recruitment of a CD40 signaling pathway in dendritic cells by B7-DC cross-linking antibody modulates T cell functions.
2	19399172	One such phenotype, the B7-DC XAb-induced antigen accumulation in mTLR-matured DCs, has been linked to signaling through TREM-2, but the signals required for other DC phenotypes critical for the therapeutic effects in animal models remain unclear.
3	19399172	Here, FRET and co-immunoprecipitation studies show that CD40 is recruited to the multi-molecular complex by B7-DC XAb.
4	19399172	Signals emanating from CD40 are important, as CD40(-/-) DCs treated with B7-DC XAb (DC(XAb)) activated DAP12, but failed to activate NFkappaB, and were not protected from cell death upon cytokine withdrawal or treatment with Vitamin D(3).
5	19399172	CD40(-/-) DC(XAb) also failed to secrete IL-6 and were unable to support the conversion of T regulatory cells into IL-17+ effector T cells in vitro.
6	19399172	Importantly, the expression of CD40 was required for the overall ability of B7-DC XAb to induce anti-tumor CTL, to provide protection from a number of tumor types, and for DC(XAb) to be effective anti-tumor vaccines in vivo.
7	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
8	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
9	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
10	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
11	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
12	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
13	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
14	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
15	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
16	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
17	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
18	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
19	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
20	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
21	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
22	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
23	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
24	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
25	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
26	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
27	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
28	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
29	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
30	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
31	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
32	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
33	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
34	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
35	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
36	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
37	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
38	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
39	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
40	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
41	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
42	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
43	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
44	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
45	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
46	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
47	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
48	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
49	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
50	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
51	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
52	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
53	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
54	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
55	20640189	Dual induction of TREM2 and tolerance-related transcript, Tmem176b, in amyloid transgenic mice: implications for vaccine-based therapies for Alzheimer's disease.
56	20640189	In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellular tolerance-associated transcript, Tmem176b (transmembrane domain protein 176b).
57	20640189	Tmem176b expression was highest in the inner zone of amyloid plaques, whereas TREM2 expression was highest in the outer zone.
58	20640189	Induced expression of TREM2 occurred co-incident with detection of thioflavine-S-positive amyloid deposits.
59	20640189	Transfection studies revealed that expression of TREM2 correlated negatively with motility, but correlated positively with the ability of microglia to stimulate CD4(+) T-cell proliferation, TNF (tumour necrosis factor) and CCL2 (chemokine ligand 2) production, but not IFNgamma (interferon gamma) production.
60	20640189	TREM2 expression also showed a positive correlation with amyloid phagocytosis in unactivated cells.
61	20640189	However, activating cells with LPS (lipopolysaccharide), but not IFNgamma, reduced the correlation between TREM2 expression and phagocytosis.
62	20640189	Taken together, these data suggest that, in vivo, Tmem176b(+) cells in closest apposition to amyloid may be the least able to clear amyloid.
63	24475103	The E7 peptide up-modulated immune response (KPNA7, IGSF6, NCR3, TREM2, TUBAL3, IL8, NFKBIA), pro-apoptosis (BTG1, SEMA6A, IGFBP3 and SRGN), anti-apoptosis (NFKBIA), DNA repair (MRPS11, RAD21, TXNRD1), and cell adhesion and cell migration genes (EPHA1, PGF, IL8 and CYR61) in iDCs.
64	26021803	Evidence for TLR4 and FcRγ-CARD9 activation by cholera toxin B subunit and its direct bindings to TREM2 and LMIR5 receptors.
65	26021803	Indeed, CTX-induced IL-6 production was substantially reduced in MyD88(-/-) or TLR4(-/-) macrophages.
66	26021803	CTB targeted not only GM1 and TLR4 but also TREM2 and LMIR5/CD300b.
67	26021803	CTB-TREM2 interaction initiated signal transduction through adaptor protein DAP12.
68	26021803	In summary, CTB targets TLR4, FcRγ-CARD9, TREM2, and LMIR5.
69	26021803	Evidence for TLR4 and FcRγ-CARD9 activation by cholera toxin B subunit and its direct bindings to TREM2 and LMIR5 receptors.
70	26021803	Indeed, CTX-induced IL-6 production was substantially reduced in MyD88(-/-) or TLR4(-/-) macrophages.
71	26021803	CTB targeted not only GM1 and TLR4 but also TREM2 and LMIR5/CD300b.
72	26021803	CTB-TREM2 interaction initiated signal transduction through adaptor protein DAP12.
73	26021803	In summary, CTB targets TLR4, FcRγ-CARD9, TREM2, and LMIR5.
74	26021803	Evidence for TLR4 and FcRγ-CARD9 activation by cholera toxin B subunit and its direct bindings to TREM2 and LMIR5 receptors.
75	26021803	Indeed, CTX-induced IL-6 production was substantially reduced in MyD88(-/-) or TLR4(-/-) macrophages.
76	26021803	CTB targeted not only GM1 and TLR4 but also TREM2 and LMIR5/CD300b.
77	26021803	CTB-TREM2 interaction initiated signal transduction through adaptor protein DAP12.
78	26021803	In summary, CTB targets TLR4, FcRγ-CARD9, TREM2, and LMIR5.
79	26021803	Evidence for TLR4 and FcRγ-CARD9 activation by cholera toxin B subunit and its direct bindings to TREM2 and LMIR5 receptors.
80	26021803	Indeed, CTX-induced IL-6 production was substantially reduced in MyD88(-/-) or TLR4(-/-) macrophages.
81	26021803	CTB targeted not only GM1 and TLR4 but also TREM2 and LMIR5/CD300b.
82	26021803	CTB-TREM2 interaction initiated signal transduction through adaptor protein DAP12.
83	26021803	In summary, CTB targets TLR4, FcRγ-CARD9, TREM2, and LMIR5.