TCCR Antibody
- Known as:
- TCCR Antibody
- Catalog number:
- 2481
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TCCR Antibody
Related genes to: TCCR Antibody
- Gene:
- IL27RA NIH gene
- Name:
- interleukin 27 receptor subunit alpha
- Previous symbol:
- -
- Synonyms:
- WSX-1, TCCR, CRL1, WSX1, zcytor1, IL-27R
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2016-10-11
Related products to: TCCR Antibody
Related articles to: TCCR Antibody
- This study aimed to examine the mechanisms by which Interleukin-27 (IL-27) contributes to the pathogenesis of oral squamous cell carcinoma (OSCC) through focal adhesion-induced stemness protein 1 (FSIP1)-mediated activation of the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway. - Source: PubMed
Publication date: 2026/03/05
Wang Qing-MeiWang Xue-YingLin FeiGuan Wei-QunChen Wei-Hui - Statins are widely used in the treatment of hyperlipidemia; however, their specific mechanisms of action remain incompletely understood. To identify key therapeutic targets, we integrated differential expression analysis with machine learning and identified IL27RA as a pivotal candidate. IL27RA expression was significantly upregulated in atorvastatin-treated hyperlipidemia patients compared to healthy controls but decreased following statin intervention. Functional enrichment analysis revealed its association with immune-related pathways, and consistent with this, immune infiltration analysis showed significant correlations between IL27RA expression and the abundance of Th1 and plasmacytoid dendritic cells. Molecular docking and dynamics simulations further confirmed stable binding between IL27RA and atorvastatin. Collectively, these results establish IL27RA as a key therapeutic target for statins in hyperlipidemia and highlight its role in modulating the immune microenvironment. - Source: PubMed
Publication date: 2026/01/05
Zhao NaLi YanLiu Yajie - Psoriasis and atopic dermatitis (AD) are two prevalent inflammatory skin disorders, each characterized by distinct adaptive immune responses. However, recent evidence suggests that these diseases may share overlapping immune mechanisms, especially concerning keratinocyte function. The specific cytokines that coordinate these inflammatory pathways remain largely undefined. - Source: PubMed
Publication date: 2026/01/07
Chen ZeyuCui LianLan ZhiyiLin SuyangYang NanLi SiqiZhao ZihanCai JiangluyiWang YuanyuanLiu TongYu YingyuanLu JiajingZhang XilinGuo ChunyuanGu JunYu QianShi Yuling - Immune checkpoint blockade (ICB) has improved outcomes for patients with triple-negative breast cancer (TNBC), yet resistance remains widespread and its molecular basis is not fully understood. Through single-cell RNA sequencing (scRNA-seq) of paired pre- and post-treatment tumor samples from patients who failed to achieve pathological complete response (non-pCR) after neoadjuvant PD-1 therapy, we identified a marked upregulation of interleukin-27 receptor subunit alpha (IL27RA) in malignant epithelial cells within residual lesions. Integration with scRNA-seq profiles from an independent cohort of three pCR patients showed that this IL27RA upregulation in malignant epithelium is largely restricted to non-pCR residual tumors, and high IL27RA expression correlated with poor survival in TNBC cohorts. Mechanistically, IL27RA suppresses MHC-I expression by activating the PI3K/AKT pathway-rather than the classical IL-27/STAT axis-thereby impairing CD8⁺ T-cell cytotoxic function. Inhibition of AKT reversed this phenotype and restored antigen-specific killing. In orthotopic tumor models, mimicking systemic loss of Il27ra significantly reduced tumor growth and prolonged survival in immunocompetent mice, with single-cell profiling indicating enhanced intratumoral T-cell and NK-cell effector activity. Collectively, our findings identify an epithelial-intrinsic IL27RA-PI3K/AKT-MHC-I axis as a central driver of immune evasion and ICB resistance in TNBC and support IL27RA as a promising therapeutic target for overcoming immunotherapy resistance. - Source: PubMed
Publication date: 2026/01/04
Xu JiachiLong QianZhou MeirongChen QitongPeng JingLiang QingchunZhang DanhuaZhou HuiYi Wenjun - Neonatal necrotizing enterocolitis (NEC) is a life-threatening gastrointestinal disease of premature infants, characterized by immune dysregulation and compromised intestinal barrier integrity. Interleukin-27 receptor α (IL-27Ra), a critical component of the JAK-STAT signaling pathway, exhibits dual pro- and anti-inflammatory roles in various inflammatory conditions. However, its role in NEC pathogenesis remains unclear. To elucidate the functional role of IL-27Ra in NEC development and assess its potential as a therapeutic target. A multi-tiered approach was employed, including integrative analysis of clinical NEC specimens by single-cell and bulk RNA sequencing, and a neonatal mouse NEC model. NEC was induced in mice via hyperosmolar formula feeding combined with LPS gavage, intermittent hypoxia, and cold stress. Additional experiments included immunofluorescence staining for IL-27Ra, cytokine profiling (ELISA, quantitative real-time PCR (qPCR)), use of IL-27Ra knockout (IL-27Ra) mice, and histopathological scoring of intestinal injury. In NEC patient intestinal tissues, IL-27Ra expression was significantly upregulated in immune cells, with expression levels positively correlating with pro-inflammatory mediators (e.g., IL-6) and inversely correlating with barrier-associated proteins (e.g., TJP1). In the neonatal mouse NEC model, genetic ablation of IL-27Ra (IL-27Ra) led to reduced histopathology scores, decreased IL-6 production (ELISA and qPCR), and restored tight junction protein expression (TJP1, OCLN). IL-27Ra promotes NEC by amplifying intestinal inflammation and damaging the mucosal barrier. Thus, IL-27Ra is identified as a promising therapeutic target. Pharmacological blockade of IL-27Ra signaling may provide a dual benefit in NEC-mitigating excessive inflammation while restoring barrier integrity. These findings are primarily derived from NEC mouse models and await clinical validation. - Source: PubMed
Publication date: 2025/11/28
Yang YulingLiu YingyanZhong LimeiYan ChunZhong XinLan ChaotingLi SitaoLiu Yufeng