Human Interleukin 23,IL-23 ELISA Kit
- Known as:
- Human Interleukin 23,Interleukin-23 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- CK-E10077
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- Eastbio
- Gene target:
- Human Interleukin 23 IL-23 ELISA Kit
Related genes to: Human Interleukin 23,IL-23 ELISA Kit
- Gene:
- IL23A NIH gene
- Name:
- interleukin 23 subunit alpha
- Previous symbol:
- -
- Synonyms:
- SGRF, IL23P19, IL-23, IL-23A, P19
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2016-10-11
Related products to: Human Interleukin 23,IL-23 ELISA Kit
Related articles to: Human Interleukin 23,IL-23 ELISA Kit
- Psoriasis is a chronic skin disease manifesting scaly, indurated erythema and an enhanced interleukin (IL)-23/IL-17 immune axis. A high-salt diet (HSD) is known to promote several autoimmune or autoinflammatory diseases. We examined whether an HSD might exacerbate topical imiquimod (IMQ)-induced psoriasis-like dermatitis in mice. Balb/c female mice were fed a normal diet (ND, 0.2% NaCl) or an HSD (4.2% NaCl) for 3 weeks, and 25 mg IMQ was applied to shaved back skin for 5 consecutive days. Compared to ND, the HSD exacerbated IMQ-induced psoriasiform dermatitis with increased scale, skin thickness, and total scores, and histologically enhanced epidermal thickening, hyperkeratosis, and dermal inflammatory infiltrates, including Ly6G+ neutrophils and CD3+ T cells. HSD increased mRNA levels of , , , , , , , , , and in IMQ-induced dermatitis. HSD increased the immunostaining areas of whole and Ser 422-phosphorylated forms of serum- and glucocorticoid-inducible kinase 1 (SGK1) in epidermal keratinocytes and dermal-infiltrating cells in IMQ-induced dermatitis. Intraperitoneal SGK1 inhibitor EMD638683 reversed the above effects of HSD in exacerbating IMQ-induced dermatitis. Our present results indicate that HSD may exacerbate murine IMQ-induced psoriasis-like dermatitis at least partially through the activation of SGK1. - Source: PubMed
Publication date: 2026/09/13
Yoshida MaiHagino TeppeiYoneyama ManamiSaeki HidehisaKanda Naoko - Transcriptional factor B lymphocyte-induced maturation protein 1 (Blimp-1) is pivotally implicated in T helper 17 (Th17) cell differentiation. This study investigated expression of the Blimp-1 protein, positive regulatory domain 1 (PRDM1), and cytokine genes in psoriasis (PsO). Affected (AS-PsO) and non-affected skin (nAS-PsO) samples were used to assess gene and protein expressions by reverse transcription-quantitative PCR (RT-qPCR), and immunostaining and confocal microscopy, respectively; the normalised public transcriptomic data permitted differential gene expression analyses. On RT-qPCR, PRDM1 and IL17A transcripts showed higher expression in AS-PsO than in nAS-PsO (n = 34) (p < 0.001; p < 0.0001, respectively). Confocal microscopy showed Blimp-1 protein expression in epidermal layer keratinocytes in AS-PsO, but not in nAS-PsO. Bioinformatic analysis of the transcriptomic dataset GSE13355 corroborated the increased PRDM1, signal transducer and activator of transcription 3 (STAT3), IL12B, TNF, IL17A, IL6, IL1B, IL22, and IL10 gene expression in AS-PsO, when compared to normal skin and nAS-PsO (p < 0.001). PRDM1 expression correlated positively (p < 0.0001) with that of IL17A (r = 0.7), IL1B (r = 0.67), IL12B (r = 0.6), IL6 (r = 0.59), IL22 (r = 0.53), IL23A (r = 0.47), IL21 (r = 0.47), IL27 (r = 0.34), IL23R (r = 0.32), S100 calcium binding protein A9 (r = 0.63), and lipocalin 2 (r = 0.50), and negatively with that of TGFB1 (r = - 0.28) and RORC (r = - 0.60). Blimp-1 may be critical in the pathogenesis of PsO dysregulation involving the Th17 inflammatory pathway. This knowledge may accelerate the development of new treatments. - Source: PubMed
Publication date: 2022/08/30
da Costa Lorena Carla OliveiraGardinassi Luiz GustavoVeras Flávio ProtásioMilanezi CristianeRamalho Leandra Náira ZambelliBenevides LucianaAlves-Filho José Carlosda Silva João Santanada Silva Souza Cacilda - The precise mechanism through which macroautophagy/autophagy affects psoriasis is poorly understood. Here, we found that keratinocyte (KC) autophagy, which was positively correlated with psoriatic severity in patients and mouse models and could be inhibited by mitogen-activated protein kinase (MAPK) family inactivation. The impairment of autophagic flux alleviated psoriasisform inflammation. We also found that an autophagy-based unconventional secretory pathway (autosecretion) dependent on ATG5 (autophagy related 5) and GORASP2 (golgi reassembly stacking protein 2) promoted psoriasiform KC inflammation. Moreover, the alarmin HMGB1 (high mobility group box 1) was more effective than other autosecretory proteins in regulating psoriasiform cutaneous inflammation. HMGB1 neutralization in autophagy-efficient KCs eliminated the differences in psoriasiform inflammation between KCs and KCs, and conversely, recombinant HMGB1 almost completely restored psoriasiform inflammation in KCs . These results suggest that HMGB1-associated autosecretion plays a pivotal role in cutaneous inflammation. Finally, we demonstrated that mice displayed attenuated psoriatic inflammation due to the essential crosstalk between KC-specific HMGB1-associated autosecretion and γδT cells. Thus, this study uncovered a novel autophagy mechanism in psoriasis pathogenesis, and the findings imply the clinical significance of investigating and treating psoriasis. 3-MA: 3-methyladenine; ACTB: actin beta; AGER: advanced glycosylation end-product specific receptor; Anti-HMGB1: anti-HMGB1 neutralizing antibody; Anti-IL18: anti-IL18 neutralizing antibody; Anti-IL1B: anti-IL1B neutralizing antibody; ATG5: autophagy related 5; BAF: bafilomycin A; BECN1: beclin 1; CASP1: caspase 1; CCL: C-C motif chemokine ligand; CsA: cyclosporine A; ctrl shRNA: lentivirus harboring shRNA against control; CXCL: C-X-C motif chemokine ligand; DCs: dendritic cells; DMEM: dulbecco's modified Eagle's medium; ELISA: enzyme-linked immunosorbent assay; EM: electron microscopy; FBS: fetal bovine serum; shRNA: lentivirus harboring shRNA against ; GORASP2/GRASP55: golgi reassembly stacking protein 2; GR1: a composite epitope between LY6 (lymphocyte antigen 6 complex) locus C1 and LY6 locus G6D antigens; H&E: hematoxylin and eosin; HMGB1: high mobility group box 1; shRNA: lentivirus harboring shRNA against ; IFNG/IFN-γ: interferon gamma; IL17A: interleukin 17A; IL18: interleukin 18; IL1A/IL-1α: interleukin 1 alpha; IL1B/IL-1β: interleukin 1 beta; IL22/IL-22: interleukin 22; IL23A: interleukin 23 subunit alpha; IL23R: interleukin 23 receptor; IMQ: imiquimod; ITGAM/CD11B: integrin subunit alpha M; ITGAX/CD11C: integrin subunit alpha X; IVL: involucrin; KC: keratinocyte; KD: knockdown; KO: knockout; mice: mice bearing an allele, in which exon 3 of the gene is flanked by two loxP sites; : mice bearing an flox allele, in which exon 2 to 4 of the gene is flanked by two loxP sites; mice: keratinocyte-specific knockout mice generated by mating mice with mice expressing recombinase under the control of the promoter of mice: keratinocyte-specific knockout mice generated by mating mice with mice expressing recombinase under the control of the promoter of mice: mice expressing 164-amino acid splice variant recombinase under the control of promoter of ; LAMP1: lysosomal associated membrane protein 1; LDH: lactate dehydrogenase; LORICRIN: loricrin cornified envelope precursor protein; M5: TNF, IL1A, IL17A, IL22 and OSM in combination; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MKI67: marker of proliferation Ki-67; MTT: thiazolyl blue tetrazolium bromide; NFKB/NF-κB: nuclear factor kappa B; NHEKs: primary normal human epidermal keratinocytes; NS: not significant; OSM: oncostatin M; PASI: psoriasis area and severity index; PtdIns3K: class III phosphatidylinositol 3-kinase; qRT-PCR: quantitative RT-PCR; RELA/p65: RELA proto-oncogene, NF-kB subunit; rHMGB1: recombinant HMGB1; rIL18: recombinant interleukin 18; rIL1B: recombinant interleukin 1 beta; S100A: S100 calcium binding protein A; SQSTM1/p62: sequestosome 1; T17: IL17A-producing T; TCR: T-cell receptor; KO mice: (T cell receptor delta chain) knockout mice, which show deficient receptor expression in all adult lymphoid and epithelial organs; TLR: toll-like receptor; TNF/TNF-α: tumor necrosis factor; WOR: wortmannin; WT: wild-type; γδT17 cells: IL17A-producing γδ T cells. - Source: PubMed
Publication date: 2020/02/16
Wang ZhenZhou HongZheng HuapingZhou XikunShen GuoboTeng XiuLiu XiaoZhang JunWei XiaoqiongHu ZhonglanZeng FanlianHu YawenHu JingWang XiaoyanChen ShuwenCheng JuanZhang ChenGui YiyueZou SongHao YanZhao QixiangWu WenlingZhou YifanCui KaijunHuang NongyuWei YuquanLi WeiLi Jiong - Spondyloarthritis (SpA) represents a group of inflammatory rheumatic diseases that cluster within families and possess overlapping clinical features. The pathogenesis of SpA encompasses a complex array of genetic, immunological and environmental factors. In this article, we will briefly review the genetics of PsA, and then focus on the genes that may be potentially linked either directly or indirectly to the immunopathology of the Th-17 pathway. The most consistent and dominant genetic effect of PsV and PsA is located on chromosome 6p21.3 within the major histocompatibility complex (MHC) region, which accounts for approximately one-third of the genetic contribution of PsV and PsA. To date, 36 genes have reached genome-wide significance, accounting for approximately 22% of psoriasis (PsV) heritability. Prominent genes identified via GWAS include HLA-Cw6, IL12B, IL23R, IL23A, TNIP1, TNFAIP3, LCE3B-LCE3C, TRAF3IP2, NFkBIA, FBXL19, TYK2, IFIH1, REL, and ERAP1. Genes identified in psoriatic arthritis (PsA) has largely echoed those in PsV and include HLA-B/C, HLA-B, IL-12B, IL-23R, TNIP1, TRAF3IP2, FBXL19, and REL. The lack of identified genetic susceptibility loci is largely attributed to the much smaller number of PsA patients and the greater clinical heterogeneity of PsA. Searching for different types of genetic variants such as small CNVs and/or insertions/deletions has also led to the identification of several genes with a function relative to PsV in particular including DEFB4, LCE3C_LCE3B, and IL-22 gene (exon 1). The candidate genes identified in PsV/PsA have highlighted pathways of critical importance to psoriatic disease including distinct signaling pathways comprised of barrier integrity, innate immune response and adaptive immune response, mediated primarily by Th-17 and Th-1 signalling. While GWAS studies have yielded great insights into the genes that contribute to the pathogenesis of PsV and PsA, replication in large cohorts, fine-mapping and resequencing efforts, together with functional studies of genetic variants identified, are warranted to better understand susceptibility to and progression of these diseases. That searching solely for common variants by GWAS will identify only a fraction of the entire genetic burden of disease, a concerted effort is underway to search for highly penetrant but rare disease alleles in families with PsV and PsA, using next-generation sequencing and through epigenetic investigations. - Source: PubMed
Publication date: 2014/11/22
O'Rielly Darren DRahman Proton - Th17 cells are known to be involved in several autoimmune or inflammatory diseases. In celiac disease (CD), recent studies suggest an implication of those cells in disease pathogenesis. We aimed at studying the role of genes relevant for the Th17 immune response in CD susceptibility. A total of 101 single nucleotide polymorphisms (SNPs), mainly selected to cover most of the variability present in 16 Th17-related genes (IL23R, RORC, IL6R, IL17A, IL17F, CCR6, IL6, JAK2, TNFSF15, IL23A, IL22, STAT3, TBX21, SOCS3, IL12RB1 and IL17RA), were genotyped in 735 CD patients and 549 ethnically matched healthy controls. Case-control comparisons for each SNP and for the haplotypes resulting from the SNPs studied in each gene were performed using chi-square tests. Gene-gene interactions were also evaluated following different methodological approaches. No significant results emerged after performing the appropriate statistical corrections. Our results seem to discard a relevant role of Th17 cells on CD risk. - Source: PubMed
Publication date: 2012/02/16
Medrano Luz MaríaGarcía-Magariños ManuelDema BárbaraEspino LauraMaluenda CarlosPolanco IsabelFigueredo M ÁngelesFernández-Arquero MiguelNúñez Concepción