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Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA [RNA-seq]

ABSTRACT: RNA-seq was used to explore the DEGs from control vs. CIA and CIA+LUT vs. CIA CD4+ T cell

ORGANISM(S): Mus musculus

PROVIDER: GSE293190 | GEO | 2026/02/04

REPOSITORIES: GEO

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Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA

Project description:Cut&tag was applied to explore the mechanism of NFATC2 confers Th17 cell differentiation and migration in CIA.

2026-02-04 | GSE293022 | GEO

Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA

Project description:Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA

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Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA [RNA-seq]

Project description:Luteolin inhibits Th17 cell differentiation and spinal infiltration in RA [RNA-seq]

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miRNA array analysis following gefinitib/luteolin administration to PC-3 cells

Project description:To determine if any altered miRNA expression is actually involved in the growth inhibition and/or cell death induction by luteolin and/or gefitinib, we performed miR-array analysis using RNA from PC-3 cells after 24h of treatment with 60Î¼M luteolin and/or 60Î¼M gefitinib. PC-3 cells were treated for 24h with DMSO, 60Î¼M luteolin (Lut), 60Î¼M gefitinib (Gef) or their co-administration (Lut+Gef). Each sample was run in duplicate.

2014-06-29 | E-GEOD-53178 | biostudies-arrayexpress

USP18 inhibits protective immune responses and the intracellular control of Mycobacterium tuberculosis in macrophages.

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2026-03-02 | GSE320445 | GEO

Pertussis Toxin Inhibits Encephalitogenic T-Cell Infiltration and Promotes a B-Cell-Driven Disease during Th17-EAE.

Project description:Pertussis toxin (PTX) is a required co-adjuvant for experimental autoimmune encephalomyelitis (EAE) induced by immunization with myelin antigen. However, PTX's effects on EAE induced by the transfer of myelin-specific T helper cells is not known. Therefore, we investigated how PTX affects the Th17 transfer EAE model (Th17-EAE). We found that PTX significantly reduced Th17-EAE by inhibiting chemokine-receptor-dependent trafficking of Th17 cells. Strikingly, PTX also promoted the accumulation of B cells in the CNS, suggesting that PTX alters the disease toward a B-cell-dependent pathology. To determine the role of B cells, we compared the effects of PTX on Th17-EAE in wild-type (WT) and B-cell-deficient (µMT) mice. Without PTX treatment, disease severity was equivalent between WT and µMT mice. In contrast, with PTX treatment, the µMT mice had significantly less disease and a reduction in pathogenic Th17 cells in the CNS compared to the WT mice. In conclusion, this study shows that PTX inhibits the migration of pathogenic Th17 cells, while promoting the accumulation of pathogenic B cells in the CNS during Th17-EAE. These data provide useful methodological information for adoptive-transfer Th17-EAE and, furthermore, describe another important experimental system to study the pathogenic mechanisms of B cells in multiple sclerosis.

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The flavonoid luteolin inhibits niacin-induced flush.

Project description:BACKGROUND AND PURPOSE: Sustained release niacin effectively lowers serum cholesterol, LDL and triglycerides, while raising HDL. However, 75% of patients experience cutaneous warmth and itching known as flush, leading to discontinuation. Acetylsalicylic acid (aspirin) reduces this flush only by about 30%, presumably through decreasing prostaglandin D2 (PGD2). We investigated whether niacin-induced flush in a rat model involves PGD2 and 5-HT, and the effect of certain flavonoids. EXPERIMENTAL APPROACH: Three skin temperature measurements from each ear were recorded with an infrared pyrometer for each time point immediately before i.p. injection with either niacin or a flavonoid. The temperature was then measured every 10 min for 60 min. KEY RESULTS: Niacin (7.5 mg per rat, equivalent to a human dose of 1750 mg per 80 kg) maximally increased ear temperature to 1.9+/-0.2 degrees C at 45 min. Quercetin and luteolin (4.3 mg per rat; 1000 mg per human), administered i.p. 45 min prior to niacin, inhibited the niacin effect by 96 and 88%, respectively. Aspirin (1.22 mg per rat; 325 mg per human) inhibited the niacin effect by only 30%. Niacin almost doubled plasma PGD2 and 5-HT, but aspirin reduced only PGD2 by 86%. In contrast, luteolin inhibited both plasma PGD2 and 5-HT levels by 100 and 67%, respectively. CONCLUSIONS AND IMPLICATIONS. Niacin-induced skin temperature increase is associated with PGD2 and 5-HT elevations in rats; luteolin may be a better inhibitor of niacin-induced flush because it blocks the rise in both mediators.

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Long non-coding RNA ENSMUST00000197208 promotes a shift in the Th17/Treg ratio via the P2X7R-NLRP3 inflammasome axis in collagen-induced arthritis

Project description:This study aims to define the role of long non-coding RNA ENSMUST00000197208 (lncRNA ENSMUST00000197208) and the P2X7R-NLRP3 inflammasome axis in Th17/Treg cell differentiation, then clarifying the pathological significance and regulatory mechanisms in collagen-induced arthritis (CIA). We then performed gene expression profiling analysis using data obtained from RNA-seq of spleen cells of CIA mice and healthy mice.

2022-10-11 | GSE214954 | GEO

Pim1 exacerbates inflammatory arthritis by mediating Th17 differentiation

Project description:The present study demonstrated that pim1-promoted mito-Ca2+ influx enhanced the activity of mitochondrial OXPHOS, bringing about the differentiation of Th17 and driving the pathogenic progression of inflammatory arthritis. Targeting pim1 impeded Th17 differentiation and alleviated collagen-induced arthritis (CIA) and SKG arthritis, suggesting that Pim1 is a target for the treatment of inflammatory arthritis.

2026-03-04 | GSE261671 | GEO

Erythropoietin inhibits SGK1-dependent TH17 induction and TH17-dependent kidney disease.

Project description:IL-17-producing CD4+ cells (TH17) are pathogenically linked to autoimmunity including to autoimmune kidney disease. Erythropoietin's (EPO) newly recognized immunoregulatory functions and its predominant intra-renal source suggested that EPO physiologically regulates TH17 differentiation, thereby serving as a barrier to the development of autoimmune kidney disease. Using in vitro studies of human and murine cells and in vivo models, we show that EPO ligation of its receptor (EPO-R) on CD4+ T cells directly inhibits TH17 generation and promotes trans-differentiation of TH17 into IL-17-FOXP3+CD4+ T cells. Mechanistically, EPO/EPO-R ligation abrogates upregulation of SGK1 gene expression and blocks p38 activity to prevent SGK1 phosphorylation, thereby inhibiting RORC-mediated transcription of IL-17 and IL-23 receptor genes. In a murine model of TH17-dependent aristolochic acid (ArA)-induced, interstitial kidney disease associated with reduced renal EPO production, we demonstrate that transgenic EPO overexpression or recombinant EPO (rEPO) administration limits TH17 formation and clinical/histological disease expression. EPO/EPO-R ligations on CD4+ T cells abrogate, while absence of T cell-expressed EPO-R augments, TH17 induction and clinical/histological expression of pristane-induced glomerulonephritis (associated with decreased intrarenal EPO). rEPO prevents spontaneous glomerulonephritis and TH17 generation in MRL-lpr mice. Together, our findings indicate that EPO physiologically and therapeutically modulate TH17 cells to limit expression of TH17-associated autoimmune kidney disease.

| S-EPMC6542617 | biostudies-literature

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