Mouse Interleukin-4 (IL-4) is a Th2-associated cytokine produced primarily by activated CD4⁺ T helper 2 (Th2) cells, group 2 innate lymphoid cells (ILC2s), mast cells, and basophils in mice (Mus musculus), where it plays a central role in regulating humoral immunity, allergic inflammation, and alternative macrophage activation. IL-4 signals through type I (IL-4Rα/γc) and type II (IL-4Rα/IL-13Rα1) receptor complexes, activating JAK/STAT6 pathways that drive B-cell proliferation, IgE class switching, mucus production, and suppression of Th1-associated cytokines such as IFN-γ. Murine IL-4 is extensively studied in experimental models of allergic airway disease (e.g., ovalbumin- or house dust mite–induced asthma), atopic dermatitis, helminth infection, and food allergy, where it contributes to eosinophilic inflammation, airway hyperresponsiveness, and tissue remodeling. IL-4–deficient and STAT6-deficient mouse models have been instrumental in defining mechanisms of Th2 polarization and allergic pathology. While IL-4 is protective in promoting antibody-mediated responses and parasite clearance, excessive or dysregulated IL-4 signaling can impair cell-mediated immunity against intracellular pathogens and drive chronic allergic inflammation. As both a biomarker and therapeutic target, mouse IL-4 remains central to preclinical research on Th1/Th2 immune balance, allergy pathogenesis, fibrosis, and development of cytokine-modulating therapies relevant to human inflammatory and allergic diseases.