Interleukin 13

Interleukin 13 (IL-13) is a is_associated_with::protein that in humans is encoded by the IL13 is_associated_with::gene. IL-13 was first cloned in 1993 and is located on chromosome 5q31 with a length of 1.4kb. IL-13 and IL-4 exhibit a 30% of sequence similarity and have a similar structure. IL-13 is is_associated_with::cytokine secreted by many cell types, but especially T helper type 2 (Th2) cells, that is a mediator of allergic is_associated_with::inflammation and disease.

Functions
IL-13 has effects on immune cells that are similar to those of the closely related cytokine IL-4. However, IL-13 is suspected to be a more central mediator of the physiologic changes induced by allergic inflammation in many tissues.

Although IL-13 is associated primarily with the induction of airway disease, it also has is_associated_with::anti-inflammatory properties. IL-13 induces a class of protein-degrading enzymes, known as is_associated_with::matrix metalloproteinases (MMPs), in the airways. These enzymes are required to induce egression of effete is_associated_with::parenchymal inflammatory cells into the airway lumen where they are then cleared. Among other factors, IL-13 induces these MMPs as part of a mechanism that protects against excessive allergic inflammation that predisposes to asphyxiation.

IL-13 is known to induce changes in hematopoietic cells, but these effects are probably less important than that of IL-4. Furthermore, IL-13 can induce is_associated_with::immunoglobulin E (IgE) secretion from activated human is_associated_with::B cells. Interestingly, deletion of IL-13 from mice does not markedly affect either Th2 cell development or antigen-specific IgE responses induced by potent is_associated_with::allergens. In comparison, deletion of IL-4 abrogates these responses. Thus, rather than a lymphoid cytokine, IL-13 acts more prominently as a molecular bridge linking allergic inflammatory cells to the non-immune cells in contact with them, thereby altering physiological function.

IL-13 induces its effects through a multi-subunit receptor that includes the alpha chain of the IL-4 receptor (IL-4Rα) and at least one of two known IL-13-specific binding chains. Most of the biological effects of IL-13, like those of IL-4, are linked to a single is_associated_with::transcription factor, signal transducer and activator of transcription 6 (is_associated_with::STAT6). This can be resulted from an allergic reaction brought about when facing an Ala gene.

Clinical significance
IL-13 specifically induces physiological changes in parasitized organs that are required to expel the offending organisms or their products. For example, expulsion from the gut of a variety of mouse is_associated_with::helminths requires IL-13 secreted by Th2 cells. IL-13 induces several changes in the gut that create an environment hostile to the parasite, including enhanced contractions and is_associated_with::glycoprotein hyper-secretion from gut epithelial cells, that ultimately lead to detachment of the organism from the gut wall and their removal.

The eggs of the parasite is_associated_with::Schistosoma mansoni may lodge in a variety of organs including the gut wall, liver, lung and even central nervous system, inducing the formation of is_associated_with::granulomas under the control of IL-13. Here, however, the eventual result is organ damage and often profound or even fatal disease, not resolution of the infection. An emerging concept is that IL-13 may antagonize Th1 responses that are required to resolve intracellular is_associated_with::infections. In this immune dysregulated context, marked by the recruitment of aberrantly large numbers of Th2 cells, IL-13 inhibits the ability of host immune cells to destroy is_associated_with::intracellular is_associated_with::pathogens.

IL-13 induces many features of is_associated_with::allergic lung disease, including airway hyperresponsiveness, is_associated_with::goblet cell is_associated_with::metaplasia and mucus hypersecretion, which all contribute to airway obstruction. IL-4 contributes to these physiologic changes, but is less important than IL-13. IL-13 also induces secretion of is_associated_with::chemokines that are required for recruitment of allergic effector cells to the lung. Studies of STAT6 transgenic mice suggest the interesting possibility that IL-13 signaling occurring only through the airway epithelium is required for most of these effects. While no studies have yet directly implicated IL-13 in the control of human diseases, many polymorphisms in the IL-13 gene have been shown to confer an enhanced risk of atopic respiratory diseases such as is_associated_with::asthma.