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	C19orf10	1 hits
4	CCL11	1 hits
5	CCL17	1 hits
6	CCL2	1 hits
7	CCL22	1 hits
8	CCL26	1 hits
9	CCL4	1 hits
10	CCL5	1 hits
11	CD4	1 hits
12	CLCA3	1 hits
13	CX3CL1	1 hits
14	CXCL10	1 hits
15	GATA3	1 hits
16	IFIT5	1 hits
17	IFITM5	1 hits
18	IFNA1	1 hits
19	IFNA14	1 hits
20	IFNA2	1 hits
21	IFNG	1 hits
22	IFNGR1	1 hits
23	IL10	1 hits
24	IL12A	1 hits
25	IL12B	1 hits
26	IL13RA2	1 hits
27	IL17A	1 hits
28	IL17D	1 hits
29	IL18	1 hits
30	IL1B	1 hits
31	IL1R2	1 hits
32	IL2	1 hits
33	IL22	1 hits
34	IL25	1 hits
35	IL31	1 hits
36	IL32	1 hits
37	IL33	1 hits
38	IL4	1 hits
39	IL5	1 hits
40	IL6	1 hits
41	IL8	1 hits
42	LTA	1 hits
43	MIRN125A	1 hits
44	MUC5AC	1 hits
45	MX1	1 hits
46	NEFL	1 hits
47	NFKB1	1 hits
48	NFKB2	1 hits
49	NOS2A	1 hits
50	OASL	1 hits
51	RSAD2	1 hits
52	SLC7A1	1 hits
53	SLC7A7	1 hits
54	STAT3	1 hits
55	STAT6	1 hits
56	TNF	1 hits
57	TPSAB1	1 hits

Related Sentences

#	PMID	Sentence
1	28581024	Two H-2^b restricted epitopes (Bt5_76-90 and Bt5_106-115 ) were recognized by CD4 T cells specific for Blo t 5, but no CD8 epitopes were identified.
2	28581024	In mice sensitized with Blo t 5-pulsed BMDC and challenged with intranasal Blo t 5 Bt5_76-90 and Bt5_106-115 , peptide-specific CD4 T cells were found to secrete the T helper type 2 cytokines interleukin-5 and interleukin-13.
3	27799314	Whereas R848 significantly reduced IL-5, IL-13, and IL-17, it induced IFN-γ and IL-27.
4	27799314	Whereas R848 significantly reduced IL-5, IL-13, and IL-17, it induced IFN-γ and IL-27.
5	27799314	Moreover, in vitro IL-27 enhanced secretion of IFN-γ whereas it inhibited IL-5 and IL-13, demonstrating its direct effect on attenuating Th2 responses.
6	27799314	Moreover, in vitro IL-27 enhanced secretion of IFN-γ whereas it inhibited IL-5 and IL-13, demonstrating its direct effect on attenuating Th2 responses.
7	27507682	The IL-13Rα2 receptor, known as a 'receptor antagonist' binds with high affinity to IL-13, and studies have identified that this plays a part in reducing fibrosis and the size of granulomas.
8	27507682	The IL-13Rα2 receptor, known as a 'receptor antagonist' binds with high affinity to IL-13, and studies have identified that this plays a part in reducing fibrosis and the size of granulomas.
9	27507682	A negative correlation between IL-13Rα2 and IL-13 was found, suggesting an increase in cytokine in early fibrosis.
10	27507682	A negative correlation between IL-13Rα2 and IL-13 was found, suggesting an increase in cytokine in early fibrosis.
11	27323126	In the ovarian cancer patients, the levels of Th1 factors (IL-2, IFNγ, TNFα, and IL-13) increased significantly in the sera, and IFNγ and TNFα increased significantly in the ovarian cancer tissues.
12	27323126	The levels of Th2 factors (IL-5 and IL-6) increased in the sera, but the level of IL-6 decreased significantly in the ovarian cancer tissues.
13	27071061	HPAI H5N1 virus induced excessive expression of type I IFNs (IFNA and IFNG), cytokines (IL1B, IL18, IL22, IL13, and IL12B), chemokines (CCL4, CCL19, CCL10, and CX3CL1) and IFN stimulated genes (OASL, MX1, RSAD2, IFITM5, IFIT5, GBP 1, and EIF2AK) in lung tissues.
14	27053161	Th2 cells produce Th2 cytokines such as IL-4, IL-5 and IL-13, but repress Th1 cytokine IFNγ.
15	27053161	We herein show that phosphorylation of Gata3 at Ser308, Thr315 and Ser316 induces dissociation of a histone deacetylase Hdac2 from the Gata3/Chd4 repressive complex in Th2 cells.
16	27053161	We also identify Akt1 as a Gata3-phosphorylating kinase, and the activation of Akt1 induces derepression of Tbx21 and Ifng expression in Th2 cells.
17	26976630	Group 2 innate lymphoid cells (ILC2) include IL-5- and IL-13-producing CRTh2(+)CD127(+)cells that are implicated in early protective immunity at mucosal surfaces.
18	26352148	To determine whether prediagnostic allergy-related serum proteins are associated with glioma, we conducted a nested case-control study of seven cytokines (IL4, IL13, IL5, IL6, IL10, IFNG, TGFB2), two soluble cytokine receptors (sIL4RA, sIL13RA2) and three allergy-related transcription factors (FOXP3, STAT3, STAT6) using serum specimens from the Janus Serum Bank Cohort in Oslo, Norway.
19	26352148	To determine whether prediagnostic allergy-related serum proteins are associated with glioma, we conducted a nested case-control study of seven cytokines (IL4, IL13, IL5, IL6, IL10, IFNG, TGFB2), two soluble cytokine receptors (sIL4RA, sIL13RA2) and three allergy-related transcription factors (FOXP3, STAT3, STAT6) using serum specimens from the Janus Serum Bank Cohort in Oslo, Norway.
20	26352148	We first estimated individual effects of the 12 serum proteins and then interactions between IL4 and IL13 and their receptors using conditional logistic regression.
21	26352148	We first estimated individual effects of the 12 serum proteins and then interactions between IL4 and IL13 and their receptors using conditional logistic regression.
22	26300430	Using data integration of genome-wide TF binding profiles, we defined regions with combinatorial binding of lineage-specific master TFs (T-BET, GATA3, and ROR-γt) and STATs (STAT1 and STAT4, STAT6, and STAT3) in murine T helper (Th) 1, Th2, and Th17 cells, respectively.
23	26300430	Genes associated with super-enhancers, including relevant Th-cell genes (such as Ifng in Th1, Il13 in Th2, and Il17a in Th17 cells), showed strong transcriptional activity.
24	25963922	Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells.
25	25963922	The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13.
26	25535857	Plasma cytokines were analyzed, and genotyping was conducted for 15 candidate genes involved in cytokine signaling: interferon-gamma (IFNG), IFNG receptor 1 (IFNGR1), interleukins (IL1R2, IL2, IL4, IL6, IL8, IL10, IL13, IL17A), nuclear factor of kappa light polypeptide gene enhancer in B cells (NFKB1 and NFKB2), and tumor necrosis factor alpha (TNFA).
27	25535857	Plasma cytokines were analyzed, and genotyping was conducted for 15 candidate genes involved in cytokine signaling: interferon-gamma (IFNG), IFNG receptor 1 (IFNGR1), interleukins (IL1R2, IL2, IL4, IL6, IL8, IL10, IL13, IL17A), nuclear factor of kappa light polypeptide gene enhancer in B cells (NFKB1 and NFKB2), and tumor necrosis factor alpha (TNFA).
28	25535857	After adjusting for genomic estimates of ancestry, self-reported race/ethnicity and viral load, SOI was associated with higher IL-13 plasma levels and with six single nucleotide polymorphisms (SNPs): IL1B rs1143642 and rs1143623, IL6 rs4719714, IL13 rs1295686, NFKB1 rs4648110, and TNFA rs2857602.
29	25535857	After adjusting for genomic estimates of ancestry, self-reported race/ethnicity and viral load, SOI was associated with higher IL-13 plasma levels and with six single nucleotide polymorphisms (SNPs): IL1B rs1143642 and rs1143623, IL6 rs4719714, IL13 rs1295686, NFKB1 rs4648110, and TNFA rs2857602.
30	25411767	The results showed that PE patients exhibited significantly increased expression levels of the B‑cell receptor genes LYN, CD22, SYK, BTK, PTPRC and NFAM1, whereas expression levels of FYN, FCRL4 and LAX1 were significantly decreased compared to those of the control group.
31	25411767	Expression levels of T‑cell‑dependent B‑cell‑activation genes, including EMR2, TNFSF9, CD86, ICOSLG, CD37 and CD97, were significantly upregulated in PE patients, whereas SPN mRNA expression was significantly downregulated compared with those of the control group.
32	25411767	LILRA1 and TLR9 T cell‑independent B‑cell activation mRNAs were significantly upregulated in PE patients compared with those of the control group.
33	25411767	In addition, the expression levels of B‑cell‑activation regulator genes, including CR1, LILRB4 and VAV1, were significantly increased, whereas SLAMF7 expression levels were significantly decreased in PE patients compared with those of the control group.
34	25411767	Furthermore, the expression levels of B‑cell‑activation‑associated cytokine genes demonstrated a significant upregulation of LTA and IL10 and downregulation of L1A, IFNA5, IFNA6, IFNA8, IFNA14, IL2, IL13 and IFNG in PE patients compared to those of the control group.
35	25366747	Four candidate genes of the cytokine family (IL2, IL4, IL13, and IFNG) were selected to identify Single Nucleotide Polymorphisms (SNPs) that might be associated with resistance to gastrointestinal endoparasites in goats.
36	24938282	By IHC and immunofluorescence, we confirmed IL32 protein expression in many CD3(+)CD4(+) T cells and some epidermotropic T cells in mycosis fungoides lesions.
37	24938282	Furthermore, by flow cytometry, IL32 production by circulating activated T cells in healthy individuals was found in both IFNγ(+) and IFNγ(-) cells but not in IL4(+) or IL13(+) cells.
38	24925396	Th2 cells produce interleukin (IL)-4 and IL-13, which induce immunoglobulin E production by B cells, and IL-5 that allows recruitment of eosinophils.
39	24925396	Th2 cells produce interleukin (IL)-4 and IL-13, which induce immunoglobulin E production by B cells, and IL-5 that allows recruitment of eosinophils.
40	24925396	Regulatory T (Treg) cells exhibit a CD4+ phenotype and include Foxp3-positive thymic and induced Tregs, as well as Foxp3-negative IL-10-producing cells.
41	24925396	Regulatory T (Treg) cells exhibit a CD4+ phenotype and include Foxp3-positive thymic and induced Tregs, as well as Foxp3-negative IL-10-producing cells.
42	24925396	Recently, innate lymphoid type 2 cells (ILC2) have been found to be able to produce high amounts of IL-5 and IL-13 in response to stimulation with IL-25 and IL-33 produced by non-immune cells.
43	24925396	Recently, innate lymphoid type 2 cells (ILC2) have been found to be able to produce high amounts of IL-5 and IL-13 in response to stimulation with IL-25 and IL-33 produced by non-immune cells.
44	24167278	Gata3/Ruvbl2 complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.
45	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.
46	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.
47	24167278	Gata3 directly bound to the Cdkn2c locus in an Ruvbl2-dependent manner.
48	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.
49	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.
50	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.
51	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.
52	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.
53	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.
54	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.
55	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.
56	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.
57	22621183	Intracellular expression of IL-31, IFN-γ, IL-13, IL-17 and IL-22 was measured using flow cytometry.
58	22621183	Intracellular expression of IL-31, IFN-γ, IL-13, IL-17 and IL-22 was measured using flow cytometry.
59	22621183	Many IL-31-producing T cells co-produced IL-13 and to lesser extent IL-22, but rarely IFN-γ or IL-17.
60	22621183	Many IL-31-producing T cells co-produced IL-13 and to lesser extent IL-22, but rarely IFN-γ or IL-17.
61	21176971	MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8.
62	21176971	PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10.
63	21176971	IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated.
64	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.
65	21176971	Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels.
66	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.
67	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.
68	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.
69	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.
70	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.
71	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.
72	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.
73	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.
74	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.
75	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.
76	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.
77	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.
78	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.
79	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.
80	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.
81	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.
82	19332534	Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA.
83	19332534	Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA.
84	19332534	IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22.
85	19332534	IL4 induced CCL11, CCL17, CCL22, and CCL26 mRNA, and ATRA increased the basal and IL4-stimulated expression of CCL17 and CCL22.
86	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
87	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
88	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
89	17611223	The IL-4/IL-13/Stat6 signalling pathway promotes luminal mammary epithelial cell development.
90	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.
91	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.
92	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.
93	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.
94	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.
95	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.
96	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.
97	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.
98	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.
99	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.
100	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.
101	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.