Ignet

Gene Information

Gene symbol: IL17A

Gene name: interleukin 17A

HGNC ID: 5981

Synonyms: IL-17A, IL-17

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	CAMK4	1 hits
3	CASP1	1 hits
4	CASP3	1 hits
5	CASP8	1 hits
6	CCL11	1 hits
7	CCL2	1 hits
8	CCL5	1 hits
9	CD2	1 hits
10	CD4	1 hits
11	CD40	1 hits
12	CD40LG	1 hits
13	CD80	1 hits
14	CD86	1 hits
15	CD8A	1 hits
16	CLDN1	1 hits
17	CLDN7	1 hits
18	CSF3	1 hits
19	CXCL10	1 hits
20	EGFR	1 hits
21	ELAVL1	1 hits
22	ESRRB	1 hits
23	FAS	1 hits
24	FASLG	1 hits
25	FOXP3	1 hits
26	GORASP1	1 hits
27	HIF1A	1 hits
28	ICAM1	1 hits
29	IL10	1 hits
30	IL13	1 hits
31	IL15	1 hits
32	IL17C	1 hits
33	IL17D	1 hits
34	IL17F	1 hits
35	IL1B	1 hits
36	IL1R1	1 hits
37	IL2	1 hits
38	IL23A	1 hits
39	IL4	1 hits
40	IL6	1 hits
41	INS	1 hits
42	LEP	1 hits
43	MIRN155	1 hits
44	MYD88	1 hits
45	NPHS1	1 hits
46	NPHS2	1 hits
47	PRKAA1	1 hits
48	RARA	1 hits
49	SETD2	1 hits
50	SOCS1	1 hits
51	SOD1	1 hits
52	STAT3	1 hits
53	SYNPO	1 hits
54	TGFA	1 hits
55	TLR2	1 hits
56	TLR4	1 hits
57	TNF	1 hits
58	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	34540858	Th17 cells have IL-17A and IL-17F as main cytokines with receptors expressed in most renal cells, being involved in the activation of many proinflammatory and profibrotic pathways.
2	34164430	KEGG enrichment analysis showed that the main pathways involved were AGE-RAGE, vascular endothelial growth factor, HIF-1, IL-17, relaxin signalling pathway, TNF, Fc epsilon RI, insulin resistance and other signaling pathways.
3	34159767	The aim of this study was to investigate the mechanism of interleukin-17 (IL-17) gene in renal tissues of rats suffering from adriamycin (ADM) nephropathy and its effect on the expression level of characteristic proteins, such as Podocalyxin and Nephrin, in podocytes.
4	34159767	The aim of this study was to investigate the mechanism of interleukin-17 (IL-17) gene in renal tissues of rats suffering from adriamycin (ADM) nephropathy and its effect on the expression level of characteristic proteins, such as Podocalyxin and Nephrin, in podocytes.
5	34159767	The aim of this study was to investigate the mechanism of interleukin-17 (IL-17) gene in renal tissues of rats suffering from adriamycin (ADM) nephropathy and its effect on the expression level of characteristic proteins, such as Podocalyxin and Nephrin, in podocytes.
6	34159767	The aim of this study was to investigate the mechanism of interleukin-17 (IL-17) gene in renal tissues of rats suffering from adriamycin (ADM) nephropathy and its effect on the expression level of characteristic proteins, such as Podocalyxin and Nephrin, in podocytes.
7	34159767	The expression levels of IL-17, forkhead box P3 (Foxp3), Nephrin, and Podocalyxin were detected by real-time quantitative PCR (RT-qPCR) and western blot analysis.
8	34159767	The expression levels of IL-17, forkhead box P3 (Foxp3), Nephrin, and Podocalyxin were detected by real-time quantitative PCR (RT-qPCR) and western blot analysis.
9	34159767	The expression levels of IL-17, forkhead box P3 (Foxp3), Nephrin, and Podocalyxin were detected by real-time quantitative PCR (RT-qPCR) and western blot analysis.
10	34159767	The expression levels of IL-17, forkhead box P3 (Foxp3), Nephrin, and Podocalyxin were detected by real-time quantitative PCR (RT-qPCR) and western blot analysis.
11	34159767	The percentages of Th17 cells and IL-17 levels in the ADM group were significantly higher than those in the control group, while the percentages of Treg cells, Foxp3, Nephrin, and Podocalyxin levels were significantly lower than those in the control group (P<0.05).
12	34159767	The percentages of Th17 cells and IL-17 levels in the ADM group were significantly higher than those in the control group, while the percentages of Treg cells, Foxp3, Nephrin, and Podocalyxin levels were significantly lower than those in the control group (P<0.05).
13	34159767	The percentages of Th17 cells and IL-17 levels in the ADM group were significantly higher than those in the control group, while the percentages of Treg cells, Foxp3, Nephrin, and Podocalyxin levels were significantly lower than those in the control group (P<0.05).
14	34159767	The percentages of Th17 cells and IL-17 levels in the ADM group were significantly higher than those in the control group, while the percentages of Treg cells, Foxp3, Nephrin, and Podocalyxin levels were significantly lower than those in the control group (P<0.05).
15	34159767	The percentages of Th17 cells, IL-17, Nephrin, and Podocalyxin in the transfection group were significantly higher than those in the ADM group and the negative control group, while the percentages of Treg cells and Foxp3 were significantly lower than those in the ADM group and the negative control group (P<0.05).
16	34159767	The percentages of Th17 cells, IL-17, Nephrin, and Podocalyxin in the transfection group were significantly higher than those in the ADM group and the negative control group, while the percentages of Treg cells and Foxp3 were significantly lower than those in the ADM group and the negative control group (P<0.05).
17	34159767	The percentages of Th17 cells, IL-17, Nephrin, and Podocalyxin in the transfection group were significantly higher than those in the ADM group and the negative control group, while the percentages of Treg cells and Foxp3 were significantly lower than those in the ADM group and the negative control group (P<0.05).
18	34159767	The percentages of Th17 cells, IL-17, Nephrin, and Podocalyxin in the transfection group were significantly higher than those in the ADM group and the negative control group, while the percentages of Treg cells and Foxp3 were significantly lower than those in the ADM group and the negative control group (P<0.05).
19	33571932	No significant variation was observed in Th17 cell frequency, retinoic acid receptor-related orphan nuclear receptor γt (RORɣt), signal transducer and Activator of transcription 3(STAT3), IL-17, and IL-23, while IL-21, IL-4, and IL-10 had significant increase in mRNA expression and protein level of peripheral blood mononuclear cells in IMN cases.
20	33571932	Reduction in the percentage of Treg cells was also accompanied with significantly decreased expression of Forkhead box P3(FOXP3) and Transforming growth factor beta(TGF-β) in IMN patients compared to the control group.
21	32961903	Patients with T2D showed elevated IL-1Ra, IL-6, IL-17A, G-CSF, IP-10, MIP-1α, and bFGF levels; concentrations of IL-4, IL-12, IL-15, INF-γ, and VEGF were decreased.
22	32961903	Patients with T2D showed elevated IL-1Ra, IL-6, IL-17A, G-CSF, IP-10, MIP-1α, and bFGF levels; concentrations of IL-4, IL-12, IL-15, INF-γ, and VEGF were decreased.
23	32961903	Patients with T2D showed elevated IL-1Ra, IL-6, IL-17A, G-CSF, IP-10, MIP-1α, and bFGF levels; concentrations of IL-4, IL-12, IL-15, INF-γ, and VEGF were decreased.
24	32961903	IL-6, IL-17A, G-CSF, MIP-1α, and bFGF correlated negatively with eGFR; IL-10 and VEGF demonstrated negative associations with WFDC2; no relationships with podocyte markers were found.
25	32961903	IL-6, IL-17A, G-CSF, MIP-1α, and bFGF correlated negatively with eGFR; IL-10 and VEGF demonstrated negative associations with WFDC2; no relationships with podocyte markers were found.
26	32961903	IL-6, IL-17A, G-CSF, MIP-1α, and bFGF correlated negatively with eGFR; IL-10 and VEGF demonstrated negative associations with WFDC2; no relationships with podocyte markers were found.
27	32961903	Adjusted IL-17A and MIP-1α were predictors of non-albuminuric CKD, IL-13 predicted albuminuria with preserved renal function, meanwhile, IL-6 and hsCRP were predictors of albuminuria with eGFR decline.
28	32961903	Adjusted IL-17A and MIP-1α were predictors of non-albuminuric CKD, IL-13 predicted albuminuria with preserved renal function, meanwhile, IL-6 and hsCRP were predictors of albuminuria with eGFR decline.
29	32961903	Adjusted IL-17A and MIP-1α were predictors of non-albuminuric CKD, IL-13 predicted albuminuria with preserved renal function, meanwhile, IL-6 and hsCRP were predictors of albuminuria with eGFR decline.
30	32686090	Our results showed that diabetes-associated inflammatory cytokines IFNγ and IL-17 all upregulated expression of MHC-I, MHC-II, CD80 and CD86 on the podocyte surface.
31	32537005	In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65.
32	32537005	In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65.
33	32537005	In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65.
34	32537005	However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway.
35	32537005	However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway.
36	32537005	However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway.
37	32537005	Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner.
38	32537005	Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner.
39	32537005	Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner.
40	32487989	RNA-binding proteins (RBPs) play a pivotal role in epigenetic regulation; tristetraprolin (TTP) and human antigen R (HuR) competitively bind cytokine mRNAs, exert contrasting effects on RNA stability, and drive inflammation.
41	32487989	RNA-binding proteins (RBPs) play a pivotal role in epigenetic regulation; tristetraprolin (TTP) and human antigen R (HuR) competitively bind cytokine mRNAs, exert contrasting effects on RNA stability, and drive inflammation.
42	32487989	RNA-binding proteins (RBPs) play a pivotal role in epigenetic regulation; tristetraprolin (TTP) and human antigen R (HuR) competitively bind cytokine mRNAs, exert contrasting effects on RNA stability, and drive inflammation.
43	32487989	In DKD patients and db/db mice, TTP expression was significantly decreased and HuR expression was increased in glomerular podocytes, concurrent with podocyte injury, histological signs of DKD, and augmented glomerular expression of interleukin (IL)-17 and claudin-1, which are targets of TTP and HuR, as evidenced by RNA immunoprecipitation.
44	32487989	In DKD patients and db/db mice, TTP expression was significantly decreased and HuR expression was increased in glomerular podocytes, concurrent with podocyte injury, histological signs of DKD, and augmented glomerular expression of interleukin (IL)-17 and claudin-1, which are targets of TTP and HuR, as evidenced by RNA immunoprecipitation.
45	32487989	In DKD patients and db/db mice, TTP expression was significantly decreased and HuR expression was increased in glomerular podocytes, concurrent with podocyte injury, histological signs of DKD, and augmented glomerular expression of interleukin (IL)-17 and claudin-1, which are targets of TTP and HuR, as evidenced by RNA immunoprecipitation.
46	32487989	In cultured podocytes, exposure to high ambient glucose amplified HuR expression and repressed TTP expression, upregulated IL-17 and claudin-1, and promoted podocyte injury.
47	32487989	In cultured podocytes, exposure to high ambient glucose amplified HuR expression and repressed TTP expression, upregulated IL-17 and claudin-1, and promoted podocyte injury.
48	32487989	In cultured podocytes, exposure to high ambient glucose amplified HuR expression and repressed TTP expression, upregulated IL-17 and claudin-1, and promoted podocyte injury.
49	32487989	Treatment of db/db mice with a small molecule inhibitor of GSK-3β abrogated the changes in TTP and HuR in glomeruli and mitigated the overexpression of their target genes (IL-17, claudin-1, B7-1, and MCP-1) thus also mitigating proteinuria and DKD pathology.
50	32487989	Treatment of db/db mice with a small molecule inhibitor of GSK-3β abrogated the changes in TTP and HuR in glomeruli and mitigated the overexpression of their target genes (IL-17, claudin-1, B7-1, and MCP-1) thus also mitigating proteinuria and DKD pathology.
51	32487989	Treatment of db/db mice with a small molecule inhibitor of GSK-3β abrogated the changes in TTP and HuR in glomeruli and mitigated the overexpression of their target genes (IL-17, claudin-1, B7-1, and MCP-1) thus also mitigating proteinuria and DKD pathology.
52	32090080	In the model group, the Psoriasis Area and Severity Index (PASI) scores of scaly and erythema obviously increased (p < 0.01), creatinine and blood urea nitrogen significantly increased (p < 0.01), the positive area of hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining in kidney increased (p < 0.01), malondialdehyde significantly increased with superoxide dismutase (SOD) decreased (p < 0.01), 24-hour urine protein increased and the expressions of podocin and CD2 associate protein (CD2AP) decreased (p < 0.01), and kidney/serum inflammatory factors (IL-17, IL-1β, IL-6, TNF-α, and IL-22) and TLR/NF-κB-related expression (TLR2, TLR4, MyD88, and NF-κBp65) all increased (p < 0.01).
53	31339775	Given that T helper (CD4⁺) cells expressing IL-17A (so-called Th17 cells) have recently been reported to be resistant to GC treatment, and GC resistance remains a major challenge in the management of NS, we hypothesized that Th17 cells produce a circulating factor that is capable of signaling to the podocyte and inducing deleterious phenotypic changes.
54	31339775	This demonstrated that podocytes treated with Th17 cell culture supernatant, as well as with patient disease plasma, showed significant stimulation of JNK and p38 MAPK pathways and an increase in motility, which was blocked using a JNK inhibitor.
55	31339775	We have previously shown that nephrotic plasma elicits a podocyte response via protease-activated receptor-1 (PAR-1).
56	30982673	The presence of IL-17A-expressing cells, mainly CD4⁺ and γδ lymphocytes, was associated with upregulation of proinflammatory factors, macrophage infiltration and the beginning of renal damage.
57	30783187	IL-17 deficiency also attenuated up-regulation of pro-inflammatory and pro-fibrotic genes including IL-6, TNF-α, CCL2, CXCL10 and TGF-β in diabetic kidneys.
58	30333818	Calcium calmodulin kinase IV (CaMK4) regulates multiple processes that significantly contribute to the lupus-related pathology by controlling the production of IL-2 and IL-17 by T cells, the proliferation of mesangial cells, and the function and structure of podocytes.
59	30333818	In lupus-prone mice, targeted delivery of a CaMK4 inhibitor to CD4⁺ T cells suppresses both autoimmunity and the development of nephritis.
60	29446486	Interleukin-17A participates in podocyte injury by inducing IL-1β secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.
61	29446486	Interleukin-17A participates in podocyte injury by inducing IL-1β secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.
62	29446486	Interleukin-17A participates in podocyte injury by inducing IL-1β secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.
63	29446486	Interleukin-17A participates in podocyte injury by inducing IL-1β secretion through ROS-NLRP3 inflammasome-caspase-1 pathway.
64	29446486	Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A.
65	29446486	Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A.
66	29446486	Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A.
67	29446486	Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A.
68	29446486	In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin.
69	29446486	In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin.
70	29446486	In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin.
71	29446486	In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin.
72	29446486	Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.
73	29446486	Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.
74	29446486	Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.
75	29446486	Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.
76	28879567	mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
77	28879567	Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
78	28879567	In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
79	28879567	In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
80	28879567	By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
81	28879567	Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
82	28879567	Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
83	28879567	More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
84	28879567	Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
85	28879567	Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
86	28871938	Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4⁺ and CD8⁺ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
87	28871938	Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4⁺ and CD8⁺ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
88	28871938	Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4⁺ and CD8⁺ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
89	28871938	Results Compared with the normal group, the levels of 24-hour urine protein, CD8⁺ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
90	28871938	Results Compared with the normal group, the levels of 24-hour urine protein, CD8⁺ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
91	28871938	Results Compared with the normal group, the levels of 24-hour urine protein, CD8⁺ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
92	28871938	The whole blood CD4⁺ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
93	28871938	The whole blood CD4⁺ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
94	28871938	The whole blood CD4⁺ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
95	28871938	The mechanism may be related to the regulation of CD4⁺ T and CD8⁺ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
96	28871938	The mechanism may be related to the regulation of CD4⁺ T and CD8⁺ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
97	28871938	The mechanism may be related to the regulation of CD4⁺ T and CD8⁺ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
98	28471953	Association of microRNA-155, interleukin 17A, and proteinuria in preeclampsia.
99	28339909	IL-17 and CD40 ligand synergistically stimulate the chronicity of diabetic nephropathy.
100	27640745	Renal interleukin-6 (IL-6), IL-10, IL-17 and transforming growth factor-β (TGF-β) levels, and the expression of forkhead box protein 3 (Foxp3) and retinoid-related orphan nuclear receptor γt (Rorγt) was measured.
101	27640745	Additional findings showed that ADR triggered a disordered cytokine network and abnormal expression of Foxp3 and Rorγt in rats, as reflected by increased levels of IL-6, IL-10, TGF-β, Rorγt and decreased levels of IL-10 and Foxp3.
102	27747195	There was also a decrease in the ratio of CD4⁺ to CD8⁺ T lymphocytes, due to an increase in the percentage of CD8⁺ T lymphocytes and a decrease in the percentage of CD4⁺ T lymphocytes, and a dramatic increase in the levels of IL-6 and IL-17.
103	26567290	Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis.
104	26567290	Leptin deficiency down-regulates IL-23 production in glomerular podocytes resulting in an attenuated immune response in nephrotoxic serum nephritis.
105	26567290	To clarify the role of leptin in the regulation of the IL-23/IL-17 axis and the development of kidney disease, we used a murine model of nephrotoxic serum (NTS) nephritis (NTN).
106	26567290	To clarify the role of leptin in the regulation of the IL-23/IL-17 axis and the development of kidney disease, we used a murine model of nephrotoxic serum (NTS) nephritis (NTN).
107	26567290	Cultured murine glomerular podocytes and peritoneal exudate macrophages (PEMs) were used to investigate the direct effect of leptin on IL-23 or MCP-1 production by qRT-PCR.
108	26567290	Cultured murine glomerular podocytes and peritoneal exudate macrophages (PEMs) were used to investigate the direct effect of leptin on IL-23 or MCP-1 production by qRT-PCR.
109	26567290	The Th17-dependent secondary immune response against deposited NTS in the glomeruli was totally impaired in FR-ob/obmice because of deteriorated IL-17 and proinflammatory cytokine production including IL-23 and MCP-1 in the kidney.
110	26567290	The Th17-dependent secondary immune response against deposited NTS in the glomeruli was totally impaired in FR-ob/obmice because of deteriorated IL-17 and proinflammatory cytokine production including IL-23 and MCP-1 in the kidney.
111	26567290	IL-23 was produced in glomerular podocytes in NTN mice and cultured murine glomerular podocytes produced IL-23 under leptin stimulation.
112	26567290	IL-23 was produced in glomerular podocytes in NTN mice and cultured murine glomerular podocytes produced IL-23 under leptin stimulation.
113	26567290	Induction of MCP-1 expression was observed in PEMs regardless of Ob-Rb, and the leptin signal was transduced without STAT3 phosphorylation in PEMs.
114	26567290	Induction of MCP-1 expression was observed in PEMs regardless of Ob-Rb, and the leptin signal was transduced without STAT3 phosphorylation in PEMs.
115	26567290	Leptin deficiency impairs the secondary immune response against NTS and down-regulates IL-23 production and Th17 responses in the NTN kidney, which is accompanied by decreased MCP-1 production and macrophage infiltration in the NTN kidney.
116	26567290	Leptin deficiency impairs the secondary immune response against NTS and down-regulates IL-23 production and Th17 responses in the NTN kidney, which is accompanied by decreased MCP-1 production and macrophage infiltration in the NTN kidney.
117	26334030	Protective effects were also observed after administration of IL-17F but not IL-17C or IL-17E.
118	26334030	Mechanistically, IL-17A administration suppressed phosphorylation of signal transducer and activator of transcription 3, a central mediator of fibrosis, upregulated anti-inflammatory microglia/macrophage WAP domain protein in an AMP-activated protein kinase-dependent manner and favorably modulated renal oxidative stress and AMP-activated protein kinase activation.
119	25904903	NKT cell-associated cytokines such as IL-2, IL-4, IFN-γ, and IL-17 were detected in kidney lysates of Stx2-injected WT mice with the peak around 36 h after Stx2 injection.
120	25173645	Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
121	25173645	However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
122	25173645	In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
123	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
124	24969676	MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
125	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
126	24969676	Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control.
127	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
128	24969676	MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control.
129	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
130	24969676	MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro.
131	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
132	24969676	And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17.
133	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
134	24969676	In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
135	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
136	24969676	This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
137	23108651	We investigated the role of interferon (IFN)-γ and interleukin (IL)-23 signaling.
138	23108651	We infused Ang II into IFN-γ receptor (IFN-γR) knockout mice and wild-type controls, as well as into mice treated with neutralizing antibodies against IL-23 receptor and IL-17A.
139	23108651	The glomeruli of Ang II-treated IFN-γR knockout mice exhibited fewer podocytes, less nephrin and synaptopodin staining, and impaired podocyte autophagy.
140	23108651	Thus, IFN-γ blockade, but not IL-23 receptor antibody treatment, protects from Ang II-induced cardiac damage and electric remodeling.
141	22427838	Using an adriamycin(ADM)-based model of FSGS, we found that BALB/c mice presented albuminuria and glomerular degeneration in association with a Th2-like pro-fibrogenic profile; these mice also expressed a combination of inflammatory cytokines, such as IL-4, IL-1α, IL-1β, IL-17, TNF-α, and chemokines, such as RANTES and eotaxin.
142	22427838	TGF-β analysis revealed increased levels of circulating protein and tissue transcripts in both ADM- and GSL-1-treated mice, suggesting that TGF-β could be associated with both FSGS pathology and iNKT-mediated immunosuppression; therefore, we analyzed the kidney expression of phosphorylated SMAD2/3 and SMAD7 proteins, molecules associated with the deleterious and protective effects of TGF-β, respectively.