Ask about this productRelated genes to: IL12 p40 protein
- Gene:
- IL12RB1 NIH gene
- Name:
- interleukin 12 receptor subunit beta 1
- Previous symbol:
- IL12RB
- Synonyms:
- CD212
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-14
- Date modifiied:
- 2019-04-23
Related products to: IL12 p40 protein
Related articles to: IL12 p40 protein
- The red-spotted grouper nervous necrosis virus (RGNNV) exhibits high pathogenicity in larval , yet the immune molecular mechanism remains unclear. Non-coding RNAs (ncRNAs) are vital in the host's immune responses during viral infection. However, there has been no study on ncRNA research for this species to date. We systematically identified 105 DE microRNAs (miRNAs), 157 DE long non-coding RNAs (lncRNAs) and 31 DE circular RNAs between the infection group and control group. Functional enrichment analysis revealed that these differentially expressed genes were significantly enriched in pathways associated with innate immune defense, inflammatory, and cell death, such as JAK-STAT signaling pathway, NF-κB signaling pathway, apoptosis, and necroptosis. Furthermore, the lncRNA-miRNA-mRNA interaction network involving miR-93 was constructed, which may represent a promising candidate therapy target for future investigations. This study presents the first comprehensive ncRNA transcriptome dataset of infected with RGNNV, identifies key antiviral defense and cell death-related genes and hub pathways, and thereby identifies miR-93-involved lncRNA-miRNA-mRNA network and key targeted genes () as hub molecular regulators in immune response of this species. - Source: PubMed
Publication date: 2026/08/12
Guo XiaoliGao ChengbinChen ZhangfanLu ShengWang LeiLi WenshengHe XinleiYang ChuanjunLi JianweiChen Songlin - Mendelian susceptibility to mycobacterial disease (MSMD) is a subset of inborn errors of immunity (IEIs) predisposing to clinical infections from less virulent mycobacterial species. Variants in 22 genes, particularly in IL-12Rβ1, have been identified that impair interferon-gamma (IFN-γ)-mediated immunity. We report a new rare MSMD patient with a homozygous variant who presented with severe and persistent ascites. - Source: PubMed
Publication date: 2026/08/25
Dolikhani MohammadrezaShakibamaram GhazalehRashtian ParisaSaberi MohammadReshadmanesh AzadehGhafaripour HosseinaliMoradian ElhamMahdaviani Seyed AlirezaBustamante Jacinta - Podocyte injury drives proteinuria and disease progression in lupus nephritis (LN), yet the mechanisms underlying podocyte dysfunction remain incompletely understood. - Source: PubMed
Publication date: 2026/08/24
Guo ChaohuanFu RongPan WenliangLi WeiLi HaoRubin LimorLancia Hyshem HHenderson JoelWang ShuoshuoNagalakshmi Sheethal Umeshde Amaral Antonella ArrudaVlachos IoannisAbdi RezaTsokos Maria GTsokos George C - While deficiency is classically associated with susceptibility to mycobacterial and infections, its clinical spectrum may be broader than currently documented literature. Timely recognition of atypical pleiotropic presentations can contribute to earlier diagnosis, more tailored interventions, and eventually better patient outcome. However, current literature lacks reports of hepatic involvement such as biliary strictures or intrahepatic cholestasis in -deficient patients. This case exemplifies the diagnostic odyssey of a child with a rare genetic anomaly manifesting as two seemingly unrelated pathophysiologies; the diagnosis was established through genetic testing after exhaustive evaluation excluded infectious, metabolic, and autoimmune etiologies. This case raises the possibility of atypical hepatobiliary manifestations associated with deficiency. Early genetic testing should be integrated into the diagnostic pathways with undiagnosed cholestasis, and clinicians should remain vigilant for systemic manifestations beyond the classical infectious profile. - Source: PubMed
Publication date: 2026/08/02
Ahmad NabeelRehman HooriaAmeer Muhammad HuzaifaHaide Syed JunaidAbdullah UmerAslam BilalSaifullah MuneebKhail Hamza Aka - Ustekinumab, targeting the shared p40 subunit of interleukin (IL)-12 and IL-23, is an effective therapy for Crohn's disease (CD), yet reliable predictors of response remain lacking. Given the central role of the IL-12/IL-23 axis in intestinal inflammation, we aimed to characterize the baseline mucosal expression of IL-12/IL-23 pathway components in lamina propria immune cells, and to explore their association with clinical response and remission following ustekinumab therapy. In this prospective, single-center study, biopsy-derived lamina propria mononuclear cells (LPMCs) were obtained from patients with CD prior to ustekinumab initiation. Gene expression of IL-12/IL-23 cytokine subunits and receptors was assessed by quantitative real-time PCR. Flow cytometry was performed to evaluate the distribution of T helper and innate lymphoid cell subsets and the expression of IL-23R and IL-12Rβ2. Clinical outcomes were assessed at week 16. Fifteen consecutive patients were enrolled and included in the study. At week 16, 14/15 (93.3%) and 9/15 (60.0%) of patients reached clinical response and remission, respectively. No statistically significant differences in baseline mucosal gene expression of IL-12/IL-23 pathway components were observed between remitters and non-remitters. A trend toward higher expression of receptor subunits (IL23R, IL12RB1, IL12RB2) was observed in remitters, albeit with high variability and overlapping distributions. Similarly, cytokine subunits (IL23p19, IL12/IL23p40, IL12p35) showed no consistent differential expression pattern between the groups. In contrast, flow cytometry revealed a significantly higher frequency of IL-23R-expressing Th1 cells in remitters compared with non-remitters (20.6% vs. 6.8%, = 0.009). Baseline transcriptional profiling of IL-12/IL-23 pathway components was not associated with remission following ustekinumab therapy. However, increased expression of IL-23R on mucosal Th1 cells identified a distinct immunological signature associated with clinical remission, suggesting that IL-23R expression on mucosal Th1 cells may represent a promising candidate biomarker that requires validation in larger independent cohorts. - Source: PubMed
Publication date: 2026/07/10
Onali Saradi Petrillo AmaliaFavale AgnesePillai RitaFantini Massimo Claudio