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
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
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
Schistosoma mansoni may lodge in a variety of organs including the gut wall, liver, lung and even central nervous system, inducing the formation of
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
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
intracellular pathogens. IL-13 expression has demonstrated to be increased in bronchoalveolar lavage (BAL) fluid and cells in patients with atopic mild asthma after allergen challenge. Genome-wide association studies have identified multiple polymorphisms of IL-13 and genes encoding the IL-13 receptors as associated with asthma susceptibility, bronchial hyperresponsiveness, and increased IgE levels. murine studies demonstrated that IL-13 was both necessary and sufficient to generate asthma-like Th2 responses in the mouse lung. In
type I diabetes, IL-13 antagonized cytotoxic insults to pancreatic β cells enhanced by
IL-6. In a mouse model of acetaminophen-induced liver injury eosinophil-driven
IL-4/IL-13 mediated hepatoprotective function. In severe
alcohol-associated hepatitis low plasma level of IL-13 is a predictor of short-term (90-day) mortality. However, in contrast to its short-term beneficiary effects in acute situations, chronically increased IL-13 contributes to development of fibrosis and
cirrhosis.
Dupilumab is a monoclonal antibody IL-13 and IL-4 modulator that targets the shared receptor of
IL-4 and IL-13,
IL4Rα. Since IL-4 and IL-13 have similar biological activities, dupilumab may be an effective form of treatment for asthmatic patients. == See also ==