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
- Diffuse intrinsic pontine glioma (DIPG) is a rare pediatric brain tumor with a critical unmet need due to the lack of approved, curative interventions available. The interweaving of malignant cells with normal tissue makes surgical extraction essentially impossible, and radiation provides only transient benefit. The recent ONC201 FDA approval, however, suggests DIPG therapy is tractable. Having identified overexpression of IL13Rα2 in DIPG tumor tissue versus normal brain tissue, we investigated binding of commercially available IL13Rα2 monoclonal antibodies. The top candidate antibody was used to generate a chimeric antibody, to which we conjugated deruxtecan to create a preclinical therapeutic candidate. - Source: PubMed
Publication date: 2026/05/19
Lian XiaoleiAllanson Victoria JRasmussen Samuel VChauhan ShefaliTan Guak-KimMorrow PaigeHanson KyleLian Emily BingHaight Anthony RHoshino TyujiLiu XianzhiBerlow Noah EKeller CharlesLian Yajun - Bispecific T cell engagers (BTEs) induce MHC-independent cytotoxicity by bridging T cells to tumor cells via binding a T cell-activating receptor and a tumor-associated antigen. BTEs have proven effective in hematologic malignancies and some solid tumors, yet their potential in glioblastoma (GBM) is largely unexplored. We developed a fully humanized BTE (hBTE) targeting interleukin-13 receptor alpha 2 (IL13RA2), a tumor-associated antigen widely expressed in GBM and associated with poor prognosis. In vitro, hBTE activated T cells and induced antigen-dependent cytokine release and cytotoxicity against IL13RA2-positive GBM cells. In vivo, hBTE showed robust target-specific activity and markedly prolonged survival in primary and recurrent GBM xenograft models, without detectable off-target local or systemic toxicity. Beyond GBM, hBTE also exhibited antitumor activity in IL13RA2-expressing solid tumors, demonstrating selective tumor accumulation and therapeutic efficacy in models of breast cancer brain metastases and extracranial lung cancer. This work highlights the therapeutic potential of BTEs in IL13RA2-expressing tumors and establishes a strong preclinical rationale for advancing hBTE therapy toward clinical translation in GBM and other tumors. - Source: PubMed
Publication date: 2026/04/30
Duffy Joseph TMartin-Regalado AngelaHaupt Benedikt EPogue Jacob RThakur AditiCota Manuel FierroZannikou MarkellaMisener SolKrymskaya Vera PMcCortney KathleenMiska JasonHorbinski CraigSimberg DmitriLesniak Maciej SJames Charles DStupp RogerBalyasnikova Irina V - Progressive IL-13 signaling is closely associated with liver fibrosis. Among fibrotic diseases, liver fibrosis induced by in advanced schistosomiasis is the primary driver of portal hypertension, which is the leading cause of mortality in affected patients. RNA sequencing analysis of human hepatic stellate cells revealed that was markedly upregulated in activated hepatic stellate cells and enriched in the cytokine-receptor interaction pathways, suggesting a potential role for IL-13RA2 in hepatic stellate cell activation and fibrosis progression. Based on these findings, we aimed to investigate whether IL-13RA2 also contributes to liver fibrosis during infection. In this study, we established a murine model of infection. Compared with IL-13RA1, IL-13RA2 expression was significantly increased at week 9 post-infection in mice. IL-13RA2 was enriched within fibrotic regions and increased in parallel with collagen accumulation and stellate cell activation. The phosphorylation levels of MEK and ERK changed in parallel with IL-13RA2 abundance. Furthermore, overexpression of IL-13RA2 markedly accelerated hepatic fibrogenesis, while knockdown of IL-13RA2 attenuated liver fibrosis induced by schistosomiasis the MEK/ERK pathway. Hence, IL-13RA2 may represent an effective and promising therapeutic target for the attenuation of liver fibrosis. - Source: PubMed
Publication date: 2026/04/25
Xiong RuiyanDu JiangyuanYang YuchenZhu YuxiaoNi YangyueChen LinHou MinXu ZhipengChen LuJi Minjun - Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, and durable responses to current systemic therapies is still limited. Tumor-associated endothelial cells (TECs) actively shape the immunosuppressive tumor microenvironment and contribute to therapeutic resistance, yet they remain underexploited as therapeutic targets in HCC. Interleukin-13 receptor alpha 2 (IL-13Rα2), long regarded as a decoy receptor for IL-13, has recently emerged as a context‑dependent molecule with therapeutic relevance across several malignancies. In the liver, single-cell and spatial transcriptomic studies indicate that IL-13Rα2 is highly compartmentalized and enriched within endothelial populations, offering a new explanation for previously inconsistent expression data in HCC. In this review, we summarize IL-13Rα2 biology across chronic liver disease and HCC, discuss its compartment‑specific functions, and highlight key mechanistic and translational questions. We further propose a framework for aligning IL‑13Rα2‑targeted strategies with its spatial distribution within tumors, with particular emphasis on endothelial‑directed intervention. This perspective may expand therapeutic opportunities beyond the toxicity and resistance associated with current anti-angiogenic therapies. - Source: PubMed
Publication date: 2026/04/14
Liu QiumengLi YaniTao RanYuan YueChen MinLiang JunnanSong JiaZhao JianpingYuan GuandouXu DafengXu GuopingChen JinLong Xin - Macrophages exhibit extensive tumor infiltration capacity across diverse solid malignancies, establishing macrophage-targeted immunotherapies as an emerging frontier in oncology. Genetic engineering of macrophages using chimeric antigen receptor (CAR) technology - enabling recognition and phagocytosis of neoplastic cells - is emerging as a potential therapeutic strategy against solid tumors. Human induced pluripotent stem cells (iPSCs) provide a renewable platform for the efficient differentiation of functionally competent macrophages. In this study, we engineered human iPSC-derived CAR macrophages (iCAR-M) targeting interleukin-13 receptor subunit alpha 2 (IL-13Rα2). Pan-tumor transcriptomic and immunohistochemical analyses revealed that IL-13Rα2, a tumor-associated antigen, was overexpressed in human glioblastoma (GBM), uterine carcinosarcoma (UCS), and melanoma specimens. In vitro phagocytosis assays revealed target-specific clearance of IL-13Rα2-positive tumor cells by iCAR-M. Intracranial administration of iCAR-M potently suppressed tumor growth, enhanced intratumoral cytotoxic T-cell infiltration, and prolonged the survival of humanized, immunocompetent mice bearing GBM xenografts. The administered iCAR-M maintained phagocytic capacity in vivo and acquired an M1-like pro-inflammatory phenotype. Comprehensive safety assessment revealed no detectable evidence of systemic toxicity or treatment-related neurotoxicity. Collectively, these results demonstrate the potent efficacy and favorable safety profile of iPSC-derived, IL-13Rα2-targeted CAR macrophages, supporting their therapeutic potential against solid tumors. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/04/15
Yang YingWang LujingZhang YiLyu ShuzhenRuan QianyingWang ChaoDou FeiyueLiang GongboYan GuangningWang MengruFan HaizhenQi HaoyueKong WeikaiGuo HaitaoLiu QingWang WenyingMao MinHuang YuxiZhou XinyueDuan JiayuSong WangyangHuang BangguoCheng YuhuiZhou LeiXu SenlinShen JunPing Yi-FangBian Xiu-WuHe ZhichengShi Yu