Interleukin-13 (IL-13) (IL-13)

Interleukin-13 (IL-13) is a pleiotropic cytokine primarily secreted by T-helper type 2 (Th2) cells, group 2 innate lymphoid cells (ILC2s), and mast cells, serving as a central mediator of type 2 inflammation (UniProt P35225). It exerts its biological effects by binding to a heterodimeric receptor complex composed of Interleukin-13 receptor alpha 1 (IL-13Rα1) and Interleukin-4 receptor alpha (IL-4Rα), which subsequently activates the JAK1/Tyk2 and STAT6 signaling pathways (PubMed: 12847238). This signaling cascade is critical for inducing B-cell class switching to IgE, promoting goblet cell hyperplasia and mucus production, and increasing airway hyperresponsiveness (NIH: PMC3114403). In pathological states, overproduction of IL-13 is a hallmark of allergic diseases such as asthma, atopic dermatitis, and eosinophilic esophagitis (StatPearls: NBK541037). Therapeutic strategies targeting this pathway include monoclonal antibodies like tralokinumab and lebrikizumab, which neutralize the IL-13 ligand itself, as well as dupilumab, which blocks the shared IL-4Rα subunit (DrugBank: DB12010). These interventions have shown significant efficacy in reducing exacerbations and improving lung function or skin clearance in patients with high type 2 inflammatory signatures.

Other names

IL13NC30P600Interleukin 13

Monoclonal antibodies bind to the IL-13 cytokine or its receptor subunits to prevent the formation of the signaling complex, thereby inhibiting the JAK/STAT6 pathway and reducing type 2 inflammatory gene expression (PubMed: 30111450).