Mouse IL-12 P70 ELISA kit
- Known as:
- Mouse Interleukin-12 P70 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1119
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Mouse IL-12 P70 ELISA kit
Related genes to: Mouse IL-12 P70 ELISA kit
- 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: Mouse IL-12 P70 ELISA kit
Related articles to: Mouse IL-12 P70 ELISA kit
- Monocyte-derived DC therapies programmed for robust IL-12p70 production have been associated with favorable outcomes in cancer clinical trials. However, clinical responses remain inconsistent even under standardized protocols, and the cellular basis for this variability is unknown. We leveraged single-cell multiomics to characterize two widely used DC platforms, the high-IL-12p70-producing alpha-Type-1-polarized DC (αDC1) and the IL-12p70-deficient DC induced in the presence of PGE (PGE-DC), at baseline and following rhCD40L activation. DC generated from 7 healthy participants representing the spectrum of rhCD40L-induced IL-12p70 production were profiled by transcriptome analysis with concurrent 42-plex surface proteomics, multiplex ELISA, and ELISpot quantification of IL-12p70-producing cells. While αDC1 and PGE-DC distinctly responded to rhCD40L, αDC1 alone unexpectedly comprised 3 transcriptionally and phenotypically distinct subpopulations in resting and stimulated states. Only a limited fraction of αDC1 coexpressed and (IL-12p70 producers), which was confirmed by ELISpot at the protein level. The distribution of αDC1 subclusters varied markedly between individuals and correlated with bulk cytokine and chemokine secretion profiles. Heterogeneity within αDC1 preparations may underlie inconsistent clinical trial outcomes, and identification of associated surface proteins provides a prospective strategy for subcluster enrichment to enhance DC release criteria and patient stratification for optimized therapeutic efficacy. - Source: PubMed
Publication date: 2026/05/02
DePuyt Allison EShoucair Peter E JBilben HollyMartinson Jeremy JMacatangay Bernard J CRinaldo Charles RKalinski PawelMailliard Robbie B - Cutaneous leishmaniasis (CL) caused by results in chronic skin ulceration and remains challenging to treat. While human transcriptomic studies have identified pathways driving immunopathology, the early events of infection and the molecular transitions from lesion formation to healing are still poorly understood. Here, we performed a longitudinal transcriptomic analysis of skin lesions and draining lymph nodes (dLNs) in the BALB/c ear dermal model infected with , which recapitulates features of human CL. Using bulk RNA sequencing at 2, 6, and 48 hours and at 14, 35, and 77 days post-infection, we characterized differential gene expression, pathway enrichment, and gene co-expression networks. Ulcerated mouse lesions (Day 35) recapitulated 77% of the inflammatory pathways described in human CL, with many persisting at Day 77 despite "clinical healing". Mice displayed additional upregulation of genes linked to macrophage polarization (, , ), nitric oxide metabolism (, ) and epidermal differentiation (e.g., , , , members). Gene co-expression analysis revealed stage-specific gene modules (M) associated with early innate responses (M3), tissue damage (M1), epithelial-mesenchymal transition (M4), and skin barrier remodeling (M6). A long non-coding RNA-enriched module (M2) was selectively downregulated during the ulceration. Cross-species comparison of ulcerated lesions revealed 16 conserved microRNAs and 12 shared epigenetic regulators, including , , , and , with known roles in inflammation and tissue repair, representing promising host-directed therapeutic targets. Together, this study provides a comprehensive temporal framework of host responses to and identifies actionable non-coding RNAs and epigenetic pathways with translational potential for CL therapy. - Source: PubMed
Publication date: 2026/05/12
Lobo-Silva JessicaOrge CibeleNeto Almiro Pires da SilvaRibeiro Bruno VinagreFávaro Regiane Deganda Silva Joyce KarolineSantos Sara Patrícia de OliveiraNunes SaraMoitinho-Junior Valdomiro SilveiraBarral AldinaMachado Natalia TavaresRamos Pablo Ivan PereiraKhouri RicardoFarias Leonardo Paiva - Major traumatic life events are risk factors for stress-related neuropsychiatric disorders, often accompanied by systemic inflammation, neuroinflammation, and microglial priming. As systemic inflammation, neuroinflammation, and microglial priming are considered risk factors for developing stress-related psychiatric disorders, one novel therapeutic strategy is to identify interventions that mitigate these responses. In this study, we investigated the effects of a novel soil-derived Mycolicibacterium, Mycolicibacterium sp. strain KGA-10, on in vitro immunoregulatory potential in murine bone marrow-derived dendritic cells (BMDCs) and on biomarkers of systemic inflammation, biomarkers of hippocampal neuroinflammation and microglial priming, and anxiety-like defensive behavioral responses in adult male rats exposed to inescapable tail-shock stress (IS). In Experiments 1 and 2, BMDCs were exposed to the type strain, Mycolicibacterium vaccae ATCC 15483 (0, 10, 30, 100, 300 µg/mL; Experiment 1) or M. sp. strain KGA-10 (100 µg/mL; Experiment 2) or sterile borate-buffered saline (BBS) vehicle followed, 24 h later, by exposure to lipopolysaccharide (LPS; 250 ng/mL) or a cell culture media vehicle, then, 24 h later, assessed for Il10, Il12a, and Il12b mRNA expression. Exposure of murine BMDCs to M. vaccae ATCC 15483 or M. sp. strain KGA-10 induced an immunoregulatory phenotype, characterized by increased ratios of Il10:Il12a and Il10:Il12b mRNA expression in both naïve and lipopolysaccharide- (LPS; 250 ng/mL) challenged conditions. In Experiment 3, adult male rats received weekly injections of heat-killed M. sp. strain KGA-10 (0.1 mg/0.1 mL, s.c.) or sterile BBS vehicle over three weeks prior to IS. Anxiety-like defensive behavioral responses were assessed 24 h following IS or home cage control conditions using the juvenile social exploration (JSE) test, while biomarkers of hippocampal neuroinflammation and microglial priming were assessed using real-time reverse transcription - polymerase chain reaction (real-time RT-PCR). M. sp. strain KGA-10 treatment promoted an anti-inflammatory immunophenotype, evidenced by decreased hippocampal Il12a, and decreased biomarkers of microglial priming, Nfkbia and Nlrp3 mRNA expression among rats exposed to IS, in association with prevention of IS-induced increases in anxiety-like defensive responses in the JSE test. These findings suggest that M. sp. strain KGA-10 is a promising candidate for a novel intervention for promotion of stress resilience and prevention of stress-related psychiatric disorders. - Source: PubMed
Publication date: 2026/05/12
Zhang HaotingMarquart Brandon MHolbrook Evan MWright Caelan T OZambrano Cristian AGebert Matthew JDawud Lamya'a MAndersen Nathan DKessler Lyanna RSago Saydie ACole Echo YCostanza-Chavez Gabriel WBaratta Michael VFrank Matthew GMacDonald Andrew SStamper Christopher EBohr Adam DFierer NoahLowry Christopher A - The significant economic burden of colorectal cancer (CRC) necessitates the development of innovative therapeutic approaches. Interest in the gut microbiota’s role in CRC has increased. Capecitabine, as a chemotherapy, may disrupt the balance of the intestinal microbiota. This study investigated the anticancer effects of capecitabine combined with fecal microbiota transplantation (FMT) in a CRC mouse model caused by azoxymethane and dextran sodium sulfate. FMT was achieved with fecal microbiota from healthy mice through enema. Capecitabine decreased the number and diameter of cancer foci in CRC mice, while FMT supplementation had a more noticeable impact, indicated by increased body weight and survival rate. Capecitabine significantly reduced the abundance of pathogenic bacteria in mice with CRC, such as Bacteroides, Enterorhabdus, Monoglobus, Rodentibacter, uncultured_rumen_bacterium, Turicibacter, and Streptococcus. The supplementation of FMT more effectively reversed the gut microbiota dysbiosis in CRC mice, as demonstrated by the ACE and Chao 1 indices, PCoA analysis, and enhanced normal biological pathways. Microbial dysbiosis induced immunological dysfunction in CRC mice, indicated by abnormal immune cell recruitment and excessive cytokine production. Capecitabine treatment reduced immune cell infiltration, including CD3+ T cells, CD4+ T cells, and CD49b+ NK cells, as chemotherapy often suppresses the immune system. The supplement of FMT increased the proportion of CD4+ T cells, CD49b+ NK cells, CD8+ T cells, and LY6G+ neutrophils, indicating improved immune responses against CRC. Moreover, capecitabine therapy alone reduced the overexpression of IL1a, IL6, IL12a, IL12b, IL17, IL22, FOXP3, STAT3, IFN-γ, TNF-α, TGF-β, GZMA, CXCR4, OPN, PD-1 and PD-L1. FMT supplementation resulted in a higher immune response to CRC, as it had a greater inhibitory effect on the overexpression of inflammatory cytokines and enhanced the production of IL10, IFN-γ, and CXCR4. These cytokines were positively correlated with Azospirillum_sp._47_25, Romboutsia, Lactococcus, Rikenella_sp._Marseille_P3215 and Turicibacter and negatively correlated with Parabacteroids, unclassified_Oscillospiraceae, Marvinbryantia, unclassified_Clostridia_vadinBB60_group, unclassified_Erysipelatoclostridiaceae, A2, Roseburia, Rikenellaceae_RC9_gut_group, Acetatifactor and unclassified_Clostridia. The combination of capecitabine and FMT is more effective at preventing CRC than capecitabine alone, as it reverses gut microbial abnormalities and boosts immune responses to CRC. - Source: PubMed
Publication date: 2026/03/14
Arshad MuhammadZhang Chong-YuanGao Zhan-KuiSun HuiXu Dan-QiFan Chao-YuanZhang Bo-WenGeng Jia-XinLi YangKotusov AleksandrLiu Shu-LinZhang NingMu Xiao-Qin - Systemic lupus erythematosus (SLE) is a systemic autoimmune disease involving production of autoantibodies by B cells. This study aimed at identifying novel drug targets using a computational algorithm to select targets and thereafter validate the top ranked 11 targets by siRNA knockdown in a primary B cell maturation assay. - Source: PubMed
Publication date: 2025/09/09
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