Ask about this productRelated genes to: IL13 protein
- Gene:
- IL13 NIH gene
- Name:
- interleukin 13
- Previous symbol:
- -
- Synonyms:
- P600, IL-13, ALRH, BHR1, MGC116786, MGC116788, MGC116789
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-07
- Date modifiied:
- 2016-10-05
- Gene:
- IL13RA2 NIH gene
- Name:
- interleukin 13 receptor subunit alpha 2
- Previous symbol:
- -
- Synonyms:
- IL-13R, IL13BP, CD213a2, CT19
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-26
- Date modifiied:
- 2015-12-11
Related products to: IL13 protein
Related articles to: IL13 protein
- Inflammatory bowel diseases (IBDs) are characterized by chronic intestinal inflammation, in which inflammatory fibroblasts contribute to epithelial damage and amplification of mucosal inflammation. However, the molecular mechanisms regulating their pathogenic activity remain incompletely understood. This study investigated the role of the epigenetic reader BRD4 in the differentiation and function of IL-13RA2-expressing inflammatory fibroblasts in IBD. - Source: PubMed
Frascatani RacheleSerra Mattia AlbertoIannucci AndreaColella MarcoMaresca ClaudiaMarafini IreneLolli ElisabettaSena GiorgiaDivizia AndreaGuida Andrea MartinaSica Giuseppe SigismondoMonteleone Giovanni - Interleukin-13 receptor alpha 2 (IL13RA2) is highly expressed in intestinal inflammation-associated fibroblasts (IAFs) and is associated with anti-tumor necrosis factor alpha (TNF-α) therapy resistance in inflammatory bowel disease (IBD). Because IL13RA2 inhibition ameliorates experimental colitis in mice, we investigated IL13RA2 regulation in Crohn's disease (CD)-derived primary human intestinal fibroblasts (phIFs) and the effect of anti-TNF-α infliximab and the Janus Kinase (JAK)1 inhibitor upadacitinib. Nineteen independent phIF cultures were established from CD surgical tissue, either from full tissue pieces (explant) or cell suspensions (suspension). phIFs were exposed to IL13, upadacitinib, infliximab, and/or signal transducer and activator of transcription (STAT)3/6 inhibitors. Cellular responses were assessed using viability assays, qRT-PCR, Western blotting and fluorescence microscopy. Suspension-derived phIFs exhibited higher basal IL13RA2 expression than explant-derived phIFs. IL13 strongly enhanced IL13RA2 mRNA and protein levels in phIFs. Upadacitinib effectively suppressed basal and IL13-induced IL13RA2 expression, without affecting phIF viability or proliferation. Infliximab did not reduce IL13-induced IL13RA2 expression. IL13 induced both STAT3 and STAT6 phosphorylation and STAT6 inhibition efficiently suppressed IL13-induced IL13RA2 expression, mirroring the effect of upadacitinib. These results reveal that CD-derived phIFs show marked heterogeneity in basal IL13RA2 expression, which is strongly induced by IL13 and associated with JAK1-STAT6 pathway activation, both of which are effectively suppressed by upadacitinib. This direct effect of JAK inhibition on IL13RA2 expression may contribute to its therapeutic effect in IBD. - Source: PubMed
Publication date: 2026/08/16
Wang LiWu Ruibinde Jong SofieSinnema NienkeTeunis JohanWeersma RinseBigaeva EmiliaDijkstra GerardFaber Klaas Nico - The failure of therapy in muscle invasive bladder cancer (MIBC) is primarily attributed to tumor heterogeneity and therapy resistance. We propose a novel approach targeting interleukin-13 receptor subunit alpha 2 (IL-13Rα2), which is expressed on bladder cancer (BC) cells but absent in normal urothelial cells. We investigated the therapeutic effects of WPD101a immunotoxin (IL-13-DT390) on IL-13Rα2-expressing BC cells in relation to BC cell phenotype and functional characteristics in vitro using both 2-dimensional (2D) and 3-dimensional (3D) models. Cell phenotype and IL-13Rα2 expression were assessed using flow cytometry, immunofluorescence, and Western blot analysis. The biological effects of WPD101a were evaluated by measuring cell viability and proliferation using the MTT, sulforhodamine B (SRB), CellTiter-Glo and Live/Dead assays. Apoptosis was assessed using Annexin V/propidium iodide (PI) staining, and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis of genes expression. We found that the reference BC cell lines TCC-SUP, JMSU-1 and UM-UC-3 express IL-13Rα2 at various level in contrast to RT-4, HCV-29 and 5637 cells. Cells expressing IL-13Rα2 were sensitive to WPD101a at lower concentrations in the 2D model (0.1 ng/mL) compared to the 3D model (1.0 ng/mL). IL-13Rα2-negative cells remain resistant to the immunotoxin. WPD101a induces apoptosis in BC cells expressing IL-13Rα2 as confirmed by the presence of apoptotic cells, increase the proportion of cells in the subG1 phase, and by the effector , , and initiator , genes expression. This study confirmed receptor-dependent cytotoxic effects of WPD101a and the ability and specificity to inhibit growth and apoptosis induction in MIBC cells expressing IL-13Rα2. - Source: PubMed
Publication date: 2026/06/19
Klimczak AleksandraKrawczenko AgnieszkaStamnitz SandraBielawska-Pohl AleksandraPiotrowska PaulinaGrzelenska HannaWypychowska AleksandraKisielewicz AlicjaMielecki MarcinBorowski RadoslawOlejniczak MariuszPajak-Tarnacka Beata - Glioblastoma (GBM) is the most aggressive primary malignant brain tumor, and while chimeric antigen receptor-T (CAR-T) cell therapy has shown promise, its efficacy remains limited by antigen heterogeneity and immune escape. Here, we investigated the expression of B7 homolog 3 (B7-H3), epidermal growth factor receptor (EGFR), and interleukin-13 receptor alpha 2 (IL-13RA2) in GBM tissues and cell lines. Although all three antigens were highly expressed, sustained exposure to B7-H3 CAR-T cells led to significant B7-H3 downregulation but concurrent EGFR upregulation, revealing a potential immune escape mechanism. To address this heterogeneity, we engineered T cells to express an anti-B7-H3 CAR and secrete an EGFR-targeting bispecific T-cell engager (EGFR-BsTe). These B7-H3-CAR-T-EGFR-BsTe cells exerted dual functionality: direct B7-H3-dependent cytotoxicity and recruitment of unmodified T cells via secreted EGFR-BsTe to eliminate EGFR-expressing tumor cells. Notably, EGFR-BsTe secretion promoted CAR-T cell proliferation and effector differentiation. In orthotopic GBM xenograft models, including mixed tumors with heterogeneous antigen expression, B7-H3-CAR-T-EGFR-BsTe cells demonstrated superior antitumor activity and prolonged survival compared to conventional B7-H3 CAR-T cells. Quantitative analysis revealed that EGFR-BsTe secretion abrogated EGFR upregulation and enhanced B7-H3 downregulation in a target-dependent manner; however, efficacy was diminished when the CAR-Target (B7-H3) was absent on a substantial fraction of tumor cells. Our findings suggest that arming B7-H3 CAR-T cells with EGFR-targeting bispecific engagers represents a promising strategy to overcome antigen heterogeneity and improve therapeutic outcomes for GBM patients. - Source: PubMed
Publication date: 2026/06/16
Zhang ZongliangYang NianZeng HuiChen YongdongLu HuaqingXu LongWang ZengWang GuoqingZhou LiangxueTong Aiping - Rhabdoid tumors (RT) are among the most aggressive pediatric malignancies, characterized by early onset in life, loss of SWI/SNF complex members (SMARCB1 or SMARCA4), and dismal outcomes despite multimodal therapy. Refractory and relapsing RT remain almost uniformly fatal, and targeted or immune-based approaches have yet to demonstrate clinical benefit. - Source: PubMed
Reitsam Nic GFincke Victoria EHernandez Ramirez Maria DanielaMucha MarlenaSipos EvaSiebenhüter LisaEnke Johanna SLossner MauriceVokuhl ChristianLapa ConstantinHasselblatt MartinFrühwald MichaelMärkl BrunoJohann Pascal D