Normal function · from ai-gene-review (P05112, commit 79fe13b38970) · AI-generated, not KB evidence

Interleukin-4 (IL-4) is a secreted four-helix bundle cytokine of the IL-4/IL-13 family, produced primarily by Th2 cells, basophils, mast cells, eosinophils, and group 2 innate lymphoid cells (ILC2s). It functions as the master regulator of type 2 immunity by binding the IL-4 receptor alpha chain (IL4RA) and signaling through two receptor complexes: the type I complex (IL4RA/IL2RG) on hematopoietic cells, and the type II complex (IL4RA/IL13RA1) on non-hematopoietic and some hematopoietic cells. IL-4 signals canonically through JAK1/JAK3-STAT6, leading to GATA3 induction that drives Th2 differentiation, B cell class switch recombination to IgE and IgG4, MHC class II upregulation on B cells, and M2 macrophage polarization. IL-4 also activates IRS-2/PI3K pathways contributing to cell survival and proliferation. It is a central mediator of allergic inflammation, anti-helminth defense, and various immune regulatory processes. The protein has three disulfide bonds (Cys3-Cys127, Cys24-Cys65, Cys46-Cys99) and one N-glycosylation site (Asn62). An alternatively spliced isoform (IL-4delta2) lacking exon 2 acts as a natural antagonist.

IL-4 binds the IL-4 receptor alpha chain (IL4RA) to initiate type I (IL4RA/IL2RG) and type II (IL4RA/IL13RA1) receptor complex assembly, driving JAK1/JAK3-STAT6 signaling that promotes Th2 differentiation, IgE class switching, and type 2 immune responses
IL-4 drives naive CD4+ T cell differentiation into Th2 effector cells through STAT6-dependent GATA3 induction, promoting type 2 adaptive immunity
IL-4 promotes B cell activation, proliferation, and class switch recombination to IgE and IgG4, through induction of AID expression via STAT6
IL-4 suppresses pro-inflammatory responses by inhibiting Th1 differentiation and macrophage pro-inflammatory cytokine production, promoting M2 macrophage polarization
In the knowledge base · computed from kb/ at build time

Disorders

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.

DisorderRelationshipWhere the gene appears
Brucella Melitensis Brucellosis susceptibility germline
Asthma untyped
Associated
mechanism: Type 2 Immune Response / Th2 Signaling
Atopic Dermatitis no genetic record
mechanism: Type 2 Immune Response

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.