IL4s

Interleukin-4 (IL-4) is a cytokine that plays a central role in shaping humoral and adaptive immune responses, particularly in promoting T helper 2 (Th2) differentiation and allergic-type inflammation. The term IL4s is not standard in the literature; when used, it generally refers to IL-4–related activity or the IL-4 cytokine itself rather than a distinct entity.

Sources and production: IL-4 is produced predominantly by activated CD4+ Th2 cells, but also by basophils, mast cells, eosinophils, and some macrophages. It acts locally in tissues and systemically to influence immune cell behavior and gene expression.

Receptors and signaling: IL-4 signals through the IL-4 receptor (IL-4R) complex, which exists in two forms. The type I receptor comprises IL-4Rα paired with the common γ-chain, while the type II receptor comprises IL-4Rα paired with IL-13 receptor α1. Signaling activates JAK kinases (such as JAK1 and JAK3) and the transcription factor STAT6, leading to changes in gene expression that drive downstream effects.

Biological effects: IL-4 promotes B cell class switching to IgE (and to some extent IgG subclasses in certain species), supports Th2 differentiation, and enhances pathways associated with allergic inflammation. It can suppress Th1 responses, upregulate MHC class II on some cells, and promote alternative activation of macrophages. IL-4 often acts in concert with IL-13 to shape tissue responses in mucosal and allergic contexts.

Clinical relevance: IL-4 is a key mediator in allergic diseases such as asthma and atopic dermatitis and contributes to helminth defense. Therapeutic strategies targeting IL-4 signaling, including blockade of the IL-4Rα subunit, can reduce IL-4 and IL-13 activity; such approaches include monoclonal antibodies used in treating inflammatory conditions.

History and genetics: The IL4 gene encodes the IL-4 cytokine. Polymorphisms and regulatory elements influence IL-4 production and may be linked to atopy and IgE levels. Transcription factors like GATA3 help regulate IL-4 expression during Th2 differentiation.