Interleukin-13 receptor (IL-13R)

The interleukin‑13 receptor is a cell surface protein complex that mediates cellular responses to the cytokine interleukin‑13. It consists primarily of two subunits—IL‑13Rα1 and IL‑13Rα2—which can form different functional complexes. The canonical signaling complex involves dimerization with the IL‑4Rα chain, enabling activation of JAK/STAT pathways, particularly STAT6, which drives gene expression changes associated with immune regulation, allergy, fibrosis, and cancer biology. The IL‑13Rα1/IL‑4Rα heterodimer is responsible for productive signal transduction upon ligand binding. In contrast, IL–⁠α₂ acts mainly as a decoy or high-affinity non-signaling “sink” for interleukin‐*.*.*.*.*.*.*, sequestering it away from productive signaling complexes. This property has been exploited therapeutically; notably, certain forms are highly overexpressed on malignant cells such as those found in glioblastoma multiforme but not on normal brain tissue. This makes them attractive targets for antibody-drug conjugates or immunotoxins designed to selectively kill tumor cells while sparing healthy tissue. The distribution pattern between hematopoietic versus nonhematopoietic tissues varies by subunit composition; this underlies differences in physiological function across cell types. Dysregulation or aberrant expression contributes to diseases including asthma/allergy through promotion of mucus production and airway remodeling—and cancer through altered immune surveillance. Therapeutic strategies have included direct targeting with engineered toxins fused to ligands specific for these receptors (such as cintredekin besudotox), monoclonal antibodies blocking ligand-receptor interaction, or using their presence as biomarkers guiding patient selection.

Other names

IL13RA1 (Interleukin 13 receptor subunit alpha 1)IL13RA2 (Interleukin 13 receptor subunit alpha 2)CD213a1CD213a2NR4IL13BPInterleukin 13 binding protein

Ligand-directed cytotoxicity via targeted immunotoxins or fusion proteins that bind to overexpressed interleukin‑13 receptors on tumor cells, leading to cell death or inhibition of signaling pathways involved in disease pathogenesis.