Aliases: P600, IL-13, ALRH, BHR1, MGC116786, MGC116788, MGC116789.
Interleukin-13 (IL-13) is a secreted four-alpha-helix bundle cytokine of the IL-4/IL-13 family, produced primarily by Th2 cells and type 2 innate lymphoid cells (ILC2s), with additional contributions from mast cells and basophils. IL-13 signals through the type II IL-4 receptor (IL-13Ralpha1/IL-4Ralpha heterodimer) to activate JAK1/TYK2 kinases and predominantly STAT6 transcription factor. It drives hallmark type-2 immune programs including mucus metaplasia (goblet cell hyperplasia, MUC5AC induction), IgE class switching (in cooperation with IL-4), subepithelial fibrosis, airway smooth muscle hyperresponsiveness, and epithelial barrier dysregulation. IL-13 also binds IL-13Ralpha2, a high-affinity decoy/scavenger receptor that limits signaling. IL-13 is central to the pathogenesis of asthma, atopic dermatitis, and eosinophilic esophagitis, and is the target of therapeutic antibodies (tralokinumab, lebrikizumab) and the dual IL-4/IL-13 blocker dupilumab.
Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.
| Disorder | Relationship | Where the gene appears |
|---|---|---|
| Rosacea | susceptibility | |
| Asthma |
untyped
Associated
|
mechanism: Type 2 Immune Response / Th2 Signaling
discussion: (unnamed)
|
| Atopic Dermatitis |
untyped
Associated
|
mechanism: Type 2 Immune Response
|
| Eosinophilic Esophagitis | no genetic record |
mechanism: Epithelial Type II IL-4 Receptor Signaling; Type 2 Immune Activation
|
| Mucous Membrane Pemphigoid | no genetic record |
mechanism: IL-13-Producing T Cell Infiltration of the Conjunctiva
|
Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.