Human interleukin 13 (IL-13) is a 17-kDa glycoprotein primarily produced by activated Th2 cells. IL-13 is involved in several stages of B-cell maturation and differentiation. It up-regulates CD23 and MHC class II expression, and promotes IgE isotype switching of B cells. Other activities include down-regulation of macrophage activity and inhibition of the production of pro-inflammatory cytokines and chemokines. The IL-13 gene is located on chromosome 5q31 and forms a cytokine gene cluster with IL-3, IL-5, IL-4, and GM-CSF, with IL-13 remarkably close to IL-4. The IL-13 and IL-4 genes exhibit a 30% sequence homology, have a similar structure and the same orientation suggesting that these genes arose as a duplication event during evolution. IL-13 induces its effects through a multi-subunit receptor that includes the alpha chain of the IL-4 receptor (IL-4Rα) and one of the two known IL-13-specific binding chains, designated IL-13Ra 1 and IL-13Ra 2. IL-13Ra 2 alone binds IL-13 with high affinity but is not thought to contribute to IL-13 signaling, as it has a short cytoplasmic tail that is devoid of signaling motifs. The heterodimeric complex formed by the IL-4Ra chain and the IL-13Ra 1 chain is thought to constitute the functional IL-13 receptor. Most of the biological effects of IL-13, like those of IL-4, are linked to a single transcription factor, signal transducer and activator of transcription 6 (STAT6) explaining the functional similarities between the two cytokines. Studies in mouse models of asthma have uniformly confirmed a pivotal role for STAT6 signaling pathways in the development of the allergic phenotype.
Although IL-13 is primarily produced by Th2 cells, it is also produced by a variety of other cell types including NK cells, mast cells, basophils and eosinophils which are of particular importance to the allergic response. On the other hand, regulation of IL-13 production is controlled by a variety of mediators including IL-9, IL-25, histamine, adenosine, and endothelin-1. Overexpression of either IL-9 or IL-25 in the murine lung shows the typical characteristics of an allergic reaction. The finding that neutralization of IL-13 in both of these situations completely abolished the allergic phenotype suggests that IL-9 and IL-25 may actually work through stimulation of IL-13 production.
IL-13 is associated primarily with the induction of airway disease and is often not detected in healthy human serum.
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