Ignet

Gene Information

Gene symbol: IFIH1

Gene name: interferon induced with helicase C domain 1

HGNC ID: 18873

Synonyms: MDA-5, Hlcd, MDA5, IDDM19

Related Genes

#	Gene Symbol	Number of hits
1	ADAD1	1 hits
2	AFF3	1 hits
3	AHSA1	1 hits
4	BAX	1 hits
5	C14orf181	1 hits
6	C19orf10	1 hits
7	C6orf173	1 hits
8	CAPS	1 hits
9	CAPSL	1 hits
10	CD226	1 hits
11	CD69	1 hits
12	CEACAM21	1 hits
13	CELIAC3	1 hits
14	CLEC16A	1 hits
15	CTLA4	1 hits
16	CTRB2	1 hits
17	CTSH	1 hits
18	DDX58	1 hits
19	DHX58	1 hits
20	ERBB3	1 hits
21	FCRL3	1 hits
22	FOXP3	1 hits
23	GCA	1 hits
24	HLA-A	1 hits
25	IFNG	1 hits
26	IL12B	1 hits
27	IL13	1 hits
28	IL17C	1 hits
29	IL2	1 hits
30	IL2RA	1 hits
31	INS	1 hits
32	IRF3	1 hits
33	IRF7	1 hits
34	ITPR3	1 hits
35	KCNH7	1 hits
36	MYD88	1 hits
37	NFKB1	1 hits
38	OAS1	1 hits
39	PTPN2	1 hits
40	PTPN22	1 hits
41	RIPK1	1 hits
42	SCGB1A1	1 hits
43	SCGB3A2	1 hits
44	SH2B3	1 hits
45	SIRPG	1 hits
46	SUMO4	1 hits
47	TLR3	1 hits
48	TLR4	1 hits
49	TLR7	1 hits
50	TLR8	1 hits

Related Sentences

#	PMID	Sentence
1	17559902	We also demonstrate that they express three intracellular sensors for viral RNA, the toll like receptor 3 (TLR3) gene, the retinoic acid-inducible gene I (RIG-I) and the melanoma differentiation-associated gene-5 (MDA-5), which induce type I IFN production in infected cells.
2	18285833	Therefore, genes included in this locus - IFIH1 interferon induced helicase, GCA grancalcin or the potassium channel KCNH7 - are potential candidates implicated in the pathogenesis of these autoimmune diseases, although strong linkage disequilibrium in the region hampered further localization of the etiologic gene.
3	18988535	To date the several loci involved to the T1DM development have been reliably identified by means of a number of approaches: MHC locus, VNTR within 5'-nontranscibed region of insulin (INS) gene, CTLA4 gene, encoding surface receptor of T cells, PTPN22 and PTPN2 genes, encoding tyrosine phosphatases of T lymphocytes, interleukin 2 (IL2) gene and alpha-chain of its receptor gene (IL2RA), as well as KIAA0350 gene (unknown function) and IFIH1 gene, encoding receptor of double-stranded DNA generated during viral infections.
4	18988535	Thus the protein products of MHC, INS, PTPN22 and PTPN2 genes involve in the formation in thymus of T-lymphocyte repertoire, which provides the immune defense of organism.
5	18988535	On the other hand the nonspecific activation of T cells, from that starts the autoimmune destruction of beta-cells of Langerhans islets of pancreas, in all probability, connects with the protein products of CTLA4, IL2, IL2RA genes, and, perhaps, PTPN22 and PTPN2 genes.
6	19324880	Identification of loss of function mutations in human genes encoding RIG-I and MDA5: implications for resistance to type I diabetes.
7	19324880	Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are essential for detecting viral RNA and triggering antiviral responses, including production of type I interferon.
8	19324880	We analyzed the phenotype of non-synonymous mutants of human RIG-I and MDA5 reported in databases by functional complementation in cell cultures.
9	19324880	However, the A946T mutation of MDA5, which has been implicated in type I diabetes by previous genetic analyses, affected neither dsRNA binding nor IFN gene activation.
10	19324880	Identification of loss of function mutations in human genes encoding RIG-I and MDA5: implications for resistance to type I diabetes.
11	19324880	Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are essential for detecting viral RNA and triggering antiviral responses, including production of type I interferon.
12	19324880	We analyzed the phenotype of non-synonymous mutants of human RIG-I and MDA5 reported in databases by functional complementation in cell cultures.
13	19324880	However, the A946T mutation of MDA5, which has been implicated in type I diabetes by previous genetic analyses, affected neither dsRNA binding nor IFN gene activation.
14	19324880	Identification of loss of function mutations in human genes encoding RIG-I and MDA5: implications for resistance to type I diabetes.
15	19324880	Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are essential for detecting viral RNA and triggering antiviral responses, including production of type I interferon.
16	19324880	We analyzed the phenotype of non-synonymous mutants of human RIG-I and MDA5 reported in databases by functional complementation in cell cultures.
17	19324880	However, the A946T mutation of MDA5, which has been implicated in type I diabetes by previous genetic analyses, affected neither dsRNA binding nor IFN gene activation.
18	19324880	Identification of loss of function mutations in human genes encoding RIG-I and MDA5: implications for resistance to type I diabetes.
19	19324880	Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are essential for detecting viral RNA and triggering antiviral responses, including production of type I interferon.
20	19324880	We analyzed the phenotype of non-synonymous mutants of human RIG-I and MDA5 reported in databases by functional complementation in cell cultures.
21	19324880	However, the A946T mutation of MDA5, which has been implicated in type I diabetes by previous genetic analyses, affected neither dsRNA binding nor IFN gene activation.
22	19615405	Functions of the cytoplasmic RNA sensors RIG-I and MDA-5: key regulators of innate immunity.
23	19615405	A second family of pattern recognition receptors has recently been identified, which comprises the cytoplasmic sensors of viral nucleic acids, including MDA-5, RIG-I, and LGP2.
24	19615405	Functions of the cytoplasmic RNA sensors RIG-I and MDA-5: key regulators of innate immunity.
25	19615405	A second family of pattern recognition receptors has recently been identified, which comprises the cytoplasmic sensors of viral nucleic acids, including MDA-5, RIG-I, and LGP2.
26	19747951	We presently examined expression of the intracellular viral RNA sensors, the RNA helicases RIG-I and MDA5, and documented the functionality of RIG-I in pancreatic beta cells.
27	19747951	FACS-purified rat beta cells and islet cells from wild-type or TLR3(-/-) mice were cultured with or without the RIG-I-specific ligand 5'-triphosphate single-stranded RNA (5'triP-ssRNA), the synthetic dsRNA polyI:C (PIC) or 5'OH-ssRNA (negative control); the RNA compounds were added in the medium or transfected in the cells using lipofectamine.
28	19747951	RIG-I and MDA5 expression were determined by real-time RT-PCR.
29	19747951	NF-kappaB and IFN-beta promoter activation were studied in the presence or absence of a dominant-negative form of RIG-I (DN-RIG-I).
30	19747951	Both extracellular (PICex) and intracellular (PICin) PIC increased expression of RIG-I and MDA5 in pancreatic beta cells.
31	19747951	PICin-induced NF-kappaB and IFN-beta promoter activation were prevented by the DN-RIG-I.
32	19747951	We presently examined expression of the intracellular viral RNA sensors, the RNA helicases RIG-I and MDA5, and documented the functionality of RIG-I in pancreatic beta cells.
33	19747951	FACS-purified rat beta cells and islet cells from wild-type or TLR3(-/-) mice were cultured with or without the RIG-I-specific ligand 5'-triphosphate single-stranded RNA (5'triP-ssRNA), the synthetic dsRNA polyI:C (PIC) or 5'OH-ssRNA (negative control); the RNA compounds were added in the medium or transfected in the cells using lipofectamine.
34	19747951	RIG-I and MDA5 expression were determined by real-time RT-PCR.
35	19747951	NF-kappaB and IFN-beta promoter activation were studied in the presence or absence of a dominant-negative form of RIG-I (DN-RIG-I).
36	19747951	Both extracellular (PICex) and intracellular (PICin) PIC increased expression of RIG-I and MDA5 in pancreatic beta cells.
37	19747951	PICin-induced NF-kappaB and IFN-beta promoter activation were prevented by the DN-RIG-I.
38	19747951	We presently examined expression of the intracellular viral RNA sensors, the RNA helicases RIG-I and MDA5, and documented the functionality of RIG-I in pancreatic beta cells.
39	19747951	FACS-purified rat beta cells and islet cells from wild-type or TLR3(-/-) mice were cultured with or without the RIG-I-specific ligand 5'-triphosphate single-stranded RNA (5'triP-ssRNA), the synthetic dsRNA polyI:C (PIC) or 5'OH-ssRNA (negative control); the RNA compounds were added in the medium or transfected in the cells using lipofectamine.
40	19747951	RIG-I and MDA5 expression were determined by real-time RT-PCR.
41	19747951	NF-kappaB and IFN-beta promoter activation were studied in the presence or absence of a dominant-negative form of RIG-I (DN-RIG-I).
42	19747951	Both extracellular (PICex) and intracellular (PICin) PIC increased expression of RIG-I and MDA5 in pancreatic beta cells.
43	19747951	PICin-induced NF-kappaB and IFN-beta promoter activation were prevented by the DN-RIG-I.
44	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
45	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
46	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
47	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
48	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
49	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
50	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
51	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
52	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
53	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
54	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
55	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
56	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
57	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
58	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
59	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
60	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
61	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
62	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
63	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
64	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
65	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
66	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
67	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
68	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
69	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
70	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
71	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
72	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
73	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
74	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
75	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
76	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
77	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
78	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
79	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
80	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
81	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
82	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
83	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
84	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
85	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
86	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
87	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
88	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
89	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
90	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
91	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
92	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
93	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
94	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
95	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
96	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
97	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
98	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
99	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
100	19825843	MDA5 and PTPN2, two candidate genes for type 1 diabetes, modify pancreatic beta-cell responses to the viral by-product double-stranded RNA.
101	19825843	We presently evaluated whether modulation of MDA5 and PTPN2, two candidate genes for T1D, affects beta-cell responses to double-stranded RNA (dsRNA), a by-product of viral replication.
102	19825843	INS-1E cells and primary fluorescence-activated cell sorting-purified rat beta-cells were transfected with small interference RNAs (siRNAs) targeting MDA5 or PTPN2 and subsequently exposed to intracellular synthetic dsRNA (polyinosinic-polycitidilic acid-PIC).
103	19825843	PIC increased MDA5 and PTPN2 mRNA expression, which was inhibited by the specific siRNAs.
104	19825843	PIC triggered apoptosis in INS-1E and primary beta-cells and this was augmented by PTPN2 knockdown (KD), although inhibition of MDA5 did not modify PIC-induced apoptosis.
105	19825843	In contrast, MDA5 silencing decreased PIC-induced cytokine and chemokine expression, although inhibition of PTPN2 induced minor or no changes in these inflammatory mediators.
106	19825843	These findings indicate that changes in MDA5 and PTPN2 expression modify beta-cell responses to dsRNA.
107	19825843	MDA5 regulates inflammatory signals, whereas PTPN2 may function as a defence mechanism against pro-apoptotic signals generated by dsRNA.
108	19956106	Here, 257 single-nucleotide polymorphisms (SNPs) have been genotyped in 19 candidate genes (INS, PTPN22, IL2RA, CTLA4, IFIH1, SUMO4, VDR, PAX4, OAS1, IRS1, IL4, IL4R, IL13, IL12B, CEACAM21, CAPSL, Q7Z4c4(5Q), FOXP3, EFHB) in 2300 affected sib-pair families and tested for association with T1D as part of the Type I Diabetes Genetics Consortium's candidate gene study.
109	19956106	In contrast, no convincing evidence of association was obtained for SUMO4, VDR, PAX4, OAS1, IRS1, IL4, IL4R, IL13, IL12B, CEACAM21 or CAPSL gene regions (http://www.T1DBase.org).
110	20033399	Using logistic regression, we found that single-nucleotide polymorphisms (SNPs) at the INS, PTPN22, and IFIH1 loci were associated with late-onset disease (OR (95%CI) = 0.57(0.47-0.69), p = 2.77 x 10(-9); OR (95%CI) = 1.50 (1.27-1.78), p = 3.98 x 10(-6); and OR (95%CI) = 0.81(0.71-0.93), p = 0.0028, respectively).
111	20033399	Thus, we believe the IL2/IL2R axis represents a potential therapeutic target for delaying the onset of disease.
112	20121407	We investigated (1) whether enterovirus is present at the onset of T1D in peripheral blood mononuclear cells (PBMC), plasma, throat, or stool, and (2) whether enteroviral presence is linked with HLA-DR type and/or polymorphisms in melanoma differentiation-associated gene 5 (MDA5) and 2'-5' oligoadenylate synthetase 1 (OAS1), factors of antiviral immunity.
113	20121407	To this end, PBMC, plasma, throat, and stool samples from 10 T1D patients and 20 unrelated controls were tested for the presence of enteroviruses (RT-PCR), for HLA-DR type, and polymorphisms in MDA5 and OAS1.
114	20121407	Enterovirus presence was linked with HLA-DR4, but not with polymorphisms in MDA5 or OAS1.
115	20121407	We investigated (1) whether enterovirus is present at the onset of T1D in peripheral blood mononuclear cells (PBMC), plasma, throat, or stool, and (2) whether enteroviral presence is linked with HLA-DR type and/or polymorphisms in melanoma differentiation-associated gene 5 (MDA5) and 2'-5' oligoadenylate synthetase 1 (OAS1), factors of antiviral immunity.
116	20121407	To this end, PBMC, plasma, throat, and stool samples from 10 T1D patients and 20 unrelated controls were tested for the presence of enteroviruses (RT-PCR), for HLA-DR type, and polymorphisms in MDA5 and OAS1.
117	20121407	Enterovirus presence was linked with HLA-DR4, but not with polymorphisms in MDA5 or OAS1.
118	20121407	We investigated (1) whether enterovirus is present at the onset of T1D in peripheral blood mononuclear cells (PBMC), plasma, throat, or stool, and (2) whether enteroviral presence is linked with HLA-DR type and/or polymorphisms in melanoma differentiation-associated gene 5 (MDA5) and 2'-5' oligoadenylate synthetase 1 (OAS1), factors of antiviral immunity.
119	20121407	To this end, PBMC, plasma, throat, and stool samples from 10 T1D patients and 20 unrelated controls were tested for the presence of enteroviruses (RT-PCR), for HLA-DR type, and polymorphisms in MDA5 and OAS1.
120	20121407	Enterovirus presence was linked with HLA-DR4, but not with polymorphisms in MDA5 or OAS1.
121	20931529	The IDDM1 locus, which lies within the human leukocyte antigen (HLA) and the IDDM2 locus, which is located to the insulin gene region, are two major genetic contributors of susceptibility.
122	20931529	Many other loci conferring susceptibility to autoimmune diabetes are being discovered, including PTPN22, CTLA4, IL2RA and IFIH1.
123	21270831	Analysis of the samples identified 18 SNPs (PTPN22, INS, IFIH1, SH2B3, ERBB3, CTLA4, C14orf181, CTSH, CLEC16A, CD69, ITPR3, C6orf173, SKAP2, PRKCQ, RNLS, IL27, SIRPG and CTRB2) with putative association.
124	21289206	RIG-I- and MDA5-initiated innate immunity linked with adaptive immunity accelerates beta-cell death in fulminant type 1 diabetes.
125	21328381	Infection with EV increased the gene-expression of toll-like receptor 3, interferon-β, and the intracellular helicase MDA5, involved in antiviral innate immunity, multi-fold over time, whereas poly(I:C) increased the expression of these genes transiently.
126	21403398	Here, we found that MDA5 and TLR3 are both required to prevent diabetes in mice infected with encephalomyocarditis virus strain D (EMCV-D), which has tropism for the insulin-producing β cells of the pancreas.
127	21403398	TLR3 and MDA5 controlled EMCV-D infection and diabetes by acting in hematopoietic and stromal cells, respectively, inducing IFN-I responses at kinetically distinct time points.
128	21403398	Here, we found that MDA5 and TLR3 are both required to prevent diabetes in mice infected with encephalomyocarditis virus strain D (EMCV-D), which has tropism for the insulin-producing β cells of the pancreas.
129	21403398	TLR3 and MDA5 controlled EMCV-D infection and diabetes by acting in hematopoietic and stromal cells, respectively, inducing IFN-I responses at kinetically distinct time points.
130	21805019	The sensing of ribonucleic acids (RNAs) by the monocyte/macrophage system occurs through the TLR7/8 Toll-like receptor family, the retinoic acid-inducible protein I (RIG-I), and the melanoma differentiation-associated protein-5 (MDA-5).
131	21805019	To determine whether circulating RNAs have an agonistic or antagonistic effect on the signaling pathways involved in inflammatory, apoptotic, and antiviral cascade, their effect on TLR8, RIG-I, MDA-5, MyD88, NF-KB, IRF-3, phosphoIRF-3, IRF-7, RIP, and p38 was evaluated.
132	21805019	A significantly lower level was achieved by cultivating PBMCs with circulating RNAs isolated from type 1 diabetic children, compared to the intact PBMCs, in relation to TLR-8, MDA-5, NF-KB, phospho IRF-3, and RIP, while it was higher for Bax.
133	21805019	All the metabolic stress conditions up-regulated NF-KB, Bcl-2, and Bax.
134	21805019	The sensing of ribonucleic acids (RNAs) by the monocyte/macrophage system occurs through the TLR7/8 Toll-like receptor family, the retinoic acid-inducible protein I (RIG-I), and the melanoma differentiation-associated protein-5 (MDA-5).
135	21805019	To determine whether circulating RNAs have an agonistic or antagonistic effect on the signaling pathways involved in inflammatory, apoptotic, and antiviral cascade, their effect on TLR8, RIG-I, MDA-5, MyD88, NF-KB, IRF-3, phosphoIRF-3, IRF-7, RIP, and p38 was evaluated.
136	21805019	A significantly lower level was achieved by cultivating PBMCs with circulating RNAs isolated from type 1 diabetic children, compared to the intact PBMCs, in relation to TLR-8, MDA-5, NF-KB, phospho IRF-3, and RIP, while it was higher for Bax.
137	21805019	All the metabolic stress conditions up-regulated NF-KB, Bcl-2, and Bax.
138	21805019	The sensing of ribonucleic acids (RNAs) by the monocyte/macrophage system occurs through the TLR7/8 Toll-like receptor family, the retinoic acid-inducible protein I (RIG-I), and the melanoma differentiation-associated protein-5 (MDA-5).
139	21805019	To determine whether circulating RNAs have an agonistic or antagonistic effect on the signaling pathways involved in inflammatory, apoptotic, and antiviral cascade, their effect on TLR8, RIG-I, MDA-5, MyD88, NF-KB, IRF-3, phosphoIRF-3, IRF-7, RIP, and p38 was evaluated.
140	21805019	A significantly lower level was achieved by cultivating PBMCs with circulating RNAs isolated from type 1 diabetic children, compared to the intact PBMCs, in relation to TLR-8, MDA-5, NF-KB, phospho IRF-3, and RIP, while it was higher for Bax.
141	21805019	All the metabolic stress conditions up-regulated NF-KB, Bcl-2, and Bax.
142	21826374	In addition, non-MHC genes, such as interferon-induced helicase 1 (IFIH1) and c-type lectin domain family 16, member A (CLEC16A), are also associated with the development of IgAD and some of the above diseases.
143	21844166	TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes.
144	21844166	In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling.
145	21844166	A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines.
146	21844166	However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells.
147	21844166	TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes.
148	21844166	In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling.
149	21844166	A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines.
150	21844166	However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells.
151	21844166	TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes.
152	21844166	In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling.
153	21844166	A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines.
154	21844166	However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells.
155	21844166	TLR7/9 versus TLR3/MDA5 signaling during virus infections and diabetes.
156	21844166	In this article, we discuss TLR7/9 versus TLR3/MDA5 signaling in antiviral responses and diabetes. pDCs are thought to have a critical role in antiviral defense because of their ability to rapidly secrete large amounts of IFN-I through TLR7/9 signaling.
157	21844166	A recent study demonstrates that although pDCs are a source of IFN-I in vivo, their overall contribution to viral containment is limited and time-dependent, such that additional cellular sources of IFN-I are required to fully control viral infections. dsRNA sensors, such as TLR3 and MDA5, provide another important trigger for antiviral IFN-I responses, which can be exploited to enhance immune responses to vaccines.
158	21844166	However, recent data demonstrate that IFN-I production via TLR3 and MDA5 is critical to counter diabetes caused by a virus with preferential tropism for pancreatic β-cells.
159	22654555	In particular, we discuss recent efforts aimed at refining diseases associations found within the HLA complex and implicating HLA class I as well as HLA-DPB1 loci.
160	22654555	We summarize data regarding non-HLA genes such as PTPN22, CTLA4, CD40, TSHR and TG which have been extensively studied in respect to their role in GD.
161	22654555	We review recent findings implicating variants of FCRL3 (gene for FC receptor-like-3 protein), SCGB3A2 (gene for secretory uteroglobin-related protein 1- UGRP1) as well as other unverified possible candidate genes for GD selected through their documented association with type 1 diabetes mellitus: Tenr-IL2-IL21, CAPSL (encoding calcyphosine-like protein), IFIH1(gene for interferon-induced helicase C domain 1), AFF3, CD226 and PTPN2.
162	23774118	Immunohistological examination revealed the presence of enterovirus in pancreatic islet cells and exocrine tissues and hyperexpression of pattern recognition receptors (PRRs) including melanoma differentiation-associated antigen 5 (MDA5), retinoic acid-inducible gene-I (RIG-I), Toll-like receptor (TLR)3 and TLR4, essential sensors of innate immunity, in islet cells and mononuclear cells (MNCs) infiltrating islets.
163	23774118	Islet β-cells simultaneously expressed CXC chemokine ligand 10 (CXCL10), IFN-γ and interleukin-18, indicating that these chemokines/ cytotoxic cytokines mutually amplify their cytoplasmic expression in the islet cells.
164	23774118	In addition to intrinsic pathway of cell apoptosis, the Fas and Fas ligand pathway are also involved as an extrinsic pathway of cell apoptosis.