Ignet

Gene Information

Gene symbol: IL13

Gene name: interleukin 13

HGNC ID: 5973

Synonyms: P600, IL-13, ALRH, BHR1, MGC116786, MGC116788, MGC116789

Related Genes

#	Gene Symbol	Number of hits
1	ARG1	1 hits
2	ARG2	1 hits
3	CCL11	1 hits
4	CCL17	1 hits
5	CCL2	1 hits
6	CCL22	1 hits
7	CCL26	1 hits
8	CCL5	1 hits
9	CD4	1 hits
10	CLCA3	1 hits
11	CXCL10	1 hits
12	GATA3	1 hits
13	IFNA2	1 hits
14	IFNG	1 hits
15	IL10	1 hits
16	IL12A	1 hits
17	IL15	1 hits
18	IL17A	1 hits
19	IL17D	1 hits
20	IL1B	1 hits
21	IL2	1 hits
22	IL31	1 hits
23	IL4	1 hits
24	IL5	1 hits
25	IL6	1 hits
26	IL8	1 hits
27	MUC5AC	1 hits
28	NOS2A	1 hits
29	SLC7A1	1 hits
30	SLC7A7	1 hits
31	STAT6	1 hits
32	TGFB1	1 hits
33	TNF	1 hits
34	TPSAB1	1 hits

Related Sentences

#	PMID	Sentence
1	12089714	Using amplification-refractory mutation system polymerase chain reaction, the following cytokine gene polymorphisms were determined: IL-2+166, IL-2-330, IL-15+13689, IL-15-80, TNF-A-308, TNFd3, IFN-G+874 (T(H)1-type cytokines), IL-4+33, IL-4-590, IL-6-174, IL-10-592, IL-10-819, IL-10-1082, IL-13+2043, IL-13-1055 (T(H)2 type cytokines), TGF-B1+869, and TGF-B1+915 (regulatory-type cytokines).
2	12089714	Univariate analysis showed that polymorphisms of IL-10-1082, TGF-B1+869, and HLA-DR6 were significantly related to liver graft rejection.
3	12089714	These findings suggest a role for the regulatory-type cytokine transforming growth factor-beta1 in human liver graft rejection.
4	12508169	Cytokines produced by type 2 Th (Th2) lymphocytes, such as interleukin (IL)-4, IL-5, and IL-13), predominate in membranous GN and in minimal change disease.
5	12508169	Interactions between IP-10/CXCL10, Mig/CXCL9 and I-TAC/CXCL11 and their shared receptor, CXCR3, seem to be responsible not only for Th1 cell infiltration in acute allograft rejection and in proliferative GN, but also for mesangial cell proliferation typical of the latter condition.
6	12508169	Moreover, in the kidneys of subjects suffering from chronic allograft nephropathy, IP-10/CXCL10, Mig/CXCL9 and I-TAC/CXCL11 have been found to be produced by and to act on the proxymal tubular epithelial cells, endothelial cells and smooth muscle vessel cells, suggesting their possible role in both the genesis of tubular atrophy and allograft artheriosclerosis.
7	12548511	In this article, we analyze the relationship between cytokine gene polymorphisms and in vitro tumor necrosis factor alpha (TNFalpha), interferon gamma (IFNgamma), and interleukin (IL)-10 and IL-13 production, both in liver transplant recipients and in healthy volunteers.
8	12548511	The evaluated cytokine gene polymorphisms involved TNF-A-308; TNF-d3; IFN-G+874; IL-10-1082, -819, and -592; and IL-13+2043, and -1055.
9	12548511	For healthy volunteers, we observed a relationship between polymorphisms of TNF-d3 and IL-10-1082 with in vitro production of TNFalpha and IL-10, respectively, whereas no significant associations were found for the other tested cytokine gene polymorphisms.
10	12548511	In this article, we analyze the relationship between cytokine gene polymorphisms and in vitro tumor necrosis factor alpha (TNFalpha), interferon gamma (IFNgamma), and interleukin (IL)-10 and IL-13 production, both in liver transplant recipients and in healthy volunteers.
11	12548511	The evaluated cytokine gene polymorphisms involved TNF-A-308; TNF-d3; IFN-G+874; IL-10-1082, -819, and -592; and IL-13+2043, and -1055.
12	12548511	For healthy volunteers, we observed a relationship between polymorphisms of TNF-d3 and IL-10-1082 with in vitro production of TNFalpha and IL-10, respectively, whereas no significant associations were found for the other tested cytokine gene polymorphisms.
13	15345197	Total and MTHPA-specific IgE levels were measured by the Pharmacia CAP system, and serum levels of interleukin (IL)-4, IL-13, and interferon-gamma (IFN-g) by enzyme immunoassay.
14	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
15	17611223	The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development.
16	17611223	Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage.
17	17611223	Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy.
18	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
19	17611223	The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development.
20	17611223	Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage.
21	17611223	Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy.
22	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
23	17611223	The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development.
24	17611223	Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage.
25	17611223	Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy.
26	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
27	17611223	The Th1/Th2 cytokine milieu is a key paradigm in lineage commitment, and IL-4 (Il4), IL-13 (Il13) and Stat6 are important mediators of Th2 development.
28	17611223	Thus, the Th1 cytokines IL-12 (Il12), interferon gamma (INFgamma; also known as Ifng) and Tnfalpha are downregulated concomitantly with the upregulation of the Th2 cytokines IL-4, IL-13 and IL-5 (Il5) as epithelial cells commit to the luminal lineage.
29	17611223	Moreover, we show that Th2 cytokines play a crucial role in mammary gland development in vivo, because differentiation and alveolar morphogenesis are reduced in both Stat6 and IL-4/IL-13 doubly deficient mice during pregnancy.
30	19332534	Ascaris-infected pigs had increased levels of liver mRNA for T-helper-2 (Th2)-associated cytokines, mast cell markers, and T regulatory (Treg) cells, while infected pigs given ATRA had higher IL4, IL13, CCL11, CCL26, CCL17, CCL22, and TPSB1 expression.
31	19332534	Gene expression for Th1-associated markers (IFNG, IL12B, and TBX21), the CXCR3 ligand (CXCL9), IL1B, and the putative Treg marker TNFRSF18 was also increased.
32	19332534	Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA.
33	19332534	IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22.
34	19332534	Ascaris-infected pigs had increased levels of liver mRNA for T-helper-2 (Th2)-associated cytokines, mast cell markers, and T regulatory (Treg) cells, while infected pigs given ATRA had higher IL4, IL13, CCL11, CCL26, CCL17, CCL22, and TPSB1 expression.
35	19332534	Gene expression for Th1-associated markers (IFNG, IL12B, and TBX21), the CXCR3 ligand (CXCL9), IL1B, and the putative Treg marker TNFRSF18 was also increased.
36	19332534	Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA.
37	19332534	IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22.
38	20121742	Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13.
39	20121742	In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects.
40	20121742	AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A.
41	20121742	Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13.
42	20121742	Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13.
43	20121742	In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects.
44	20121742	AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A.
45	20121742	Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13.
46	20121742	Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13.
47	20121742	In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects.
48	20121742	AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A.
49	20121742	Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13.
50	21176971	MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8.
51	21176971	PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10.
52	21176971	IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated.
53	21176971	Compared to NEG pigs, coinfection resulted in a significant increase in expression of IFNG, IL1B, IL8, CCL5, CXCL10, and weak stimulation of IFNB, IL6 and IL10; IL13 and IFNA were significantly downregulated.
54	21176971	Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels.
55	21573182	There were no differences in early IFN-g and IL-10 expression between WT and IL-13-/- mice and depletion of CD4+ T cells did not affect infection in IL-13-/- mice.
56	21573182	Collectively, these data demonstrate a lack of CD4+ T cell involvement and a novel role for IL-13 in innate responses to infection.
57	21573182	There were no differences in early IFN-g and IL-10 expression between WT and IL-13-/- mice and depletion of CD4+ T cells did not affect infection in IL-13-/- mice.
58	21573182	Collectively, these data demonstrate a lack of CD4+ T cell involvement and a novel role for IL-13 in innate responses to infection.
59	21744329	Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis.
60	21744329	The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human.
61	21744329	Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13.
62	21744329	Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis.
63	21744329	The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human.
64	21744329	Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13.
65	21744329	Assessment of the levels of nitric oxide (NO) and cytokines (IL-5, IL-6, IL-13, TNF, IFN-gamma) in giardiosis.
66	21744329	The serum concentrations of IL-5, IL-6, IL-13, TNF, IFN-g were assayed using a set of Quantikine human.
67	21744329	Patients infected with G. intestinalis showed a statistically significant increase in the levels of NO, IFN-g and IL-13.
68	22621183	Intracellular expression of IL-31, IFN-γ, IL-13, IL-17 and IL-22 was measured using flow cytometry.
69	22621183	Many IL-31-producing T cells co-produced IL-13 and to lesser extent IL-22, but rarely IFN-γ or IL-17.
70	22621183	Intracellular expression of IL-31, IFN-γ, IL-13, IL-17 and IL-22 was measured using flow cytometry.
71	22621183	Many IL-31-producing T cells co-produced IL-13 and to lesser extent IL-22, but rarely IFN-γ or IL-17.
72	23755752	Histone modifications of Notch1 promoter affect lung CD4+ T cell differentiation in asthmatic rats.
73	23755752	The present study aimed to explore the histone modifications of Notch1 promoter in normal and asthmatic lung CD4+ T cells.
74	23755752	Chromatin immunoprecipitation analysis showed that the acetylation levels of total H3, H4, site-specific H3K9, H3K14, H3K27, H3K18, H4K16, and the trimethylation levels of H3K4, H3K79 of Notch1 gene promoter were increased significantly in asthmatic lung CD4+ T cells compared to the control group, which correlated with increased P300, PCAF activity and decreased HDAC1, HDAC2 activity.
75	23755752	After intervention of garcinol, a potent inhibitor of histone acetyltransferases, in asthmatic lung CD4+ T cells, HAT activity decreased significantly and the increased Notch1 and hes-1 expression was reversed.
76	23755752	Results showed that the levels of IL-4, IL-5 and IL-13 were significantly reduced and a small reverse trend was found in the level of IFN-g after GAR treatment.
77	23761633	STAT4 and T-bet are required for the plasticity of IFN-γ expression across Th2 ontogeny and influence changes in Ifng promoter DNA methylation.
78	23761633	CD4(+) T cells developing toward a Th2 fate express IL-4, IL-5, and IL-13 while inhibiting production of cytokines associated with other Th types, such as the Th1 cytokine IFN- γ.
79	23761633	We now show that this flexibility ("plasticity") of cytokine expression is preceded by a loss of the repressive DNA methylation of the Ifng promoter acquired during Th2 polarization yet requires STAT4 along with T-box expressed in T cells.
80	23761633	Surprisingly, loss of either STAT4 or T-box expressed in T cells increased Ifng promoter CpG methylation in both effector and memory Th2 cells.
81	23831616	Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11.
82	23831616	However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected.
83	23831616	Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11.
84	23831616	However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected.
85	24167278	Gata3/Ruvbl2 complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.
86	24167278	GATA-binding protein 3 (Gata3) controls the differentiation of naive CD4 T cells into T helper 2 (Th2) cells by induction of chromatin remodeling of the Th2 cytokine gene loci, direct transactivation of Il5 and Il13 genes, and inhibition of Ifng.
87	24167278	We herein found that Gata3 associates with RuvB-like protein 2 (Ruvbl2) and represses the expression of a CDK inhibitor, cyclin-dependent kinase inhibitor 2c (Cdkn2c) to facilitate the proliferation of Th2 cells.
88	24167278	Gata3 directly bound to the Cdkn2c locus in an Ruvbl2-dependent manner.
89	24167278	We therefore have identified a functional Gata3/Ruvbl2 complex that regulates the proliferation of differentiating Th2 cells through the repression of a CDK inhibitor, Cdkn2c.