Ask about this productRelated genes to: IL23 antibody
- 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: IL23 antibody
Related articles to: IL23 antibody
- We compared the cytokine profiles between two lupus low disease activity state (LLDAS) subgroups-clinically active (CA) and serologically active clinically quiescent (SACQ)-and identified predictors of disease flare. Fifty patients with systemic lupus erythematosus (25 CA, 25 SACQ) who maintained LLDAS for ≥6 months were enrolled and followed for 6 months. Cytokine modules were identified using weighted gene co-expression network analysis, and correlations with clinical traits were assessed. Predictors of flare were assessed using Cox regression. Three cytokine modules were identified. The brown (MCP-1 and IL-8) and turquoise (IFN-α, IFN-γ, IL-17A, IL-10, IL-12p70, IL-18, IL-23A, and IL-33) modules correlated with mucocutaneous and physician global assessment, respectively. These modules showed a positive, but not significant, correlation with CA. The comparison analysis revealed that IL-6 and IL-8 were higher in CA than in SACQ. Nine patients (18%) flared, six of whom belonged to the CA group. Flares were associated with a lower sustained LLDAS rate (77.8% vs. 34.1%) and higher levels of IL-1β, IL-6, and IL-33. In multivariable analysis, non-sustained LLDAS (HR 8.73) and IL-6 ≥ 45.1 pg/mL (HR 10.4) independently predicted a flare. Our study demonstrated that cytokine elevation persists despite LLDAS. Non-sustained LLDAS and elevated IL-6 predict a flare, suggesting that IL-6 may enhance the flare prediction biomarker. - Source: PubMed
Publication date: 2026/04/28
Piriyasanguanpong WarotSiripaitoon BoonjingJuthong SiripornUea-Areewongsa ParichatIntapiboon Porntip - Sepsis is a life-threatening organ dysfunction caused by dysregulated host responses to infection. Identifying key genes associated with sepsis and exploring their interactions with immune cells are crucial for advancing diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/31
Lin ZhiyingFang WuYang Chunli - Celastrol, a bioactive compound from Tripterygium wilfordii Hook F, has been reported to exert potent anti-inflammatory effects through multiple signaling pathways. While its activity has been studied in various cell types and disease models, its effects in atopic dermatitis (AD) is limited to a few studies in mouse models and remains largely unexplored in in vitro cell models. In this study, anti-inflammatory effects of celastrol were assessed in Th1-driven 2D inflammation models of HaCaT keratinocytes and dermal fibroblasts (DF), and in a Th2-driven 3D AD skin model. Cytokine stimulation mimicked chronic inflammation. Celastrol was applied at sub-cytotoxic concentrations, and inflammatory markers were quantified on the mRNA (qPCR) and protein (ELISA) level. In 2D models, celastrol reduced interleukin (IL)-8 and IL-6 secretion in a concentration-dependent manner, with fibroblasts producing higher cytokine levels than keratinocytes. In 3D AD models, topical celastrol (10 µM) was well tolerated and markedly reduced secretion of IL-8, IL-6, IL-1α, and mRNA expression of CXCL8, IL6, IL1B, and IL23A, even under continuous Th2 stimulation. AD biomarker genes CCL26, CA2, and NELL2 were unaffected, likely due to persistent cytokine exposure. Celastrol displayed strong anti-inflammatory activity in both Th1- and Th2-driven in vitro skin inflammation models, including a physiologically relevant 3D AD model. Its multitarget action support its potential as a topical treatment candidate for chronic inflammatory skin diseases. - Source: PubMed
Publication date: 2026/04/02
Reddersen KirstenMorgner BiankaWerz OliverLorkowski StefanFischer DagmarTittelbach JörgWiegand Cornelia - High Mobility Group Box 1 (HMGB1) and Procathepsin L (pCTS-L) are crucial inflammatory mediators, yet their immunomodulating properties in human immune cells have not been systematically compared. This study employed RNA-sequencing to comparatively analyze their transcriptional effects on primary human peripheral blood mononuclear cells (PBMCs). Our findings demonstrate that while both mediators elicited significant transcriptional changes indicative of robust inflammatory responses, HMGB1 consistently induced a more extensive and diversified inflammatory program. Specifically, at a lower concentration of 0.5 µg/ml, HMGB1 triggered nearly four times more differentially expressed genes (DEGs) than pCTS-L (2.0 µg/ml). Despite this quantitative difference, an overlap of 412 DEGs (272 upregulated, 140 downregulated) revealed shared core inflammatory pathways, including the extensive upregulation of pro-inflammatory cytokines (e.g., IL1A, IL1B, and IL6), chemokines (e.g., CCL2 and CXCL1), and S100 proteins (e.g., S100A8, S100A9, and S100A12). Both mediators also converged on activating the non-canonical NF-κB pathway, evidenced by NFKB2 and RELB upregulation, suggesting a common underlying regulatory mechanism. Notably, HMGB1 uniquely upregulated CASP4 and CASP5-key components of the non-canonical inflammasome pathway-and a broader spectrum of cytokines and chemokines (e.g., IL23A, CXCL5). These findings delineate the distinct yet overlapping roles of HMGB1 and pCTS-L in orchestrating immune responses, offering a foundation for targeted therapeutic development for inflammatory diseases. - Source: PubMed
Publication date: 2026/03/16
Lou LiQiang XiaolingZhu Cassie ShuXiong BrianChen WeiqiangLi JianhuaTracey Kevin JWang Haichao - Interleukin (IL)-23 neutralizing antibodies are clinically efficacious but differ in the functionality of their Fc portion. Guselkumab (GUS) and ustekinumab (UST) have a wild-type (WT) Fc portion, permitting native binding to Fc gamma receptors (FcγRs), while risankizumab (RZB) lacks FcγR binding due to the L234A to L235A (LALA) mutation. Recently, GUS was reported to neutralize IL-23 more effectively than RZB in vitro, owing to GUS-mediated binding of FcγRI (CD64) on macrophages. However, these findings do not account for the fact that FcγRI (CD64) is competitively occupied by endogenous immunoglobulin (Ig)Gs in vivo, as it is a high-affinity receptor for monomeric IgGs. - Source: PubMed
Publication date: 2026/03/28
Cohen-Solal Joel FPohl Calvin SCummings Sheila MGygi Jeremy PSafikhani ZhalehBartocha BrigitteBuckley Christopher DDong YongliEyerich KillianKarsen Samuel DLynch Grace RMacoritto MichaelMorisset Pierre ANelson Ornella DRadstake TimothyRieder FlorianRivas JocelynSavaryn John PSmith Kathleen MStulir MadisonSzynal CarminTylek CaseyVeldman Geertruida MWasserman Laura GWestmoreland SusanChaudhary NehaStaron Matthew M