Interleukin13 (IL-13)

Interleukin 13 (IL-13) is a pleiotropic cytokine that may be important in the regulation of the inflammatory and immune responses.

Interleukin 13 (IL-13) is a protein that in humans is encoded by the IL13 gene.

IL-13 is located on chromosome 5q31.

IL-13 inhibits inflammatory cytokine production and synergies with IL-2 in regulating interferon-gamma synthesis. 

IL-13 are similar to that of Interleukin 4 (IL-4).

It has 25% sequence identity to IL-4 and is capable of IL-4 independent signaling.

IL-13 is a cytokine secreted by T helper type 2 (Th2) cells, CD4 cells, natural killer T cell, mast cells, basophils, and eosinophils.

Interleukin-13 is a central regulator in IgE synthesis, goblet cell hyperplasia, mucus hypersecretion, airway hyperresponsiveness, and fibrosis.

IL-13 mediates allergic inflammation and asthma.

Its effects on immune cells that are similar to those of the closely related cytokine IL-4.

IL-13 is suspected to be the central mediator of the physiologic changes induced by allergic inflammation in many tissues.

IL-13 is associated primarily with the induction of airway disease, it also has anti-inflammatory properties.

IL-13 induces a class of protein-degrading enzymes, known as matrix metalloproteinases (MMPs), in the airways.

These MMPs enzymes are needed to induce aggression of 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 respiratory distress.

IL-13 is known to induce changes in hematopoietic cells.

IL-13 can induce immunoglobulin IgE secretion from activated human B cells.

IL-13 acts more prominently as a molecular bridge linking allergic inflammatory cell to the non-immune cells in contact with them, thereby altering physiological function.

The signaling of IL-13 begins through a shared receptor with IL-4.

Interleukin-13 and its associated receptors with α subunit of the IL-4 receptor allows for the downstream activation of STAT6, which

regulates gene expression of cell types critical to the balance between host immune defense and allergic inflammatory responses.

Most normal cells, such as immune cells or endothelial cells, express very low or undetectable levels of IL-13 receptors.

Cell-surface expression of IL-13Rα2 on human asthmatic airway fibroblasts is  reduced compared with expression on normal control airway fibroblasts.

Interleukin-13 has a critical role in goblet cell metaplasia.

Interleukin-13 induces goblet cell differentiation and allows for the production of  mucin 5AC in tracheal epithelium, with increasing production of excessive mucus within the bronchi.

The changes in mucin storation and secretion contributes to the pathophysiologic mechanisms for various clinical abnormalities in asthmatic patients including sputum production, airway narrowing, exacerbation and accelerated loss in lung function.

IL-13 has been shown to induce a potent fibrogenic program during the course of diverse diseases marked by elevated Type 2 cytokines such as chronic schistosomiasis and atopic dermatitis among others. 

IL-13 is closely related to IL-4, and both stimulate Type 2 immunity.

IL-13 specifically induces physiological changes in organs that are required to expel the offending organisms or their products. 

IL-13 induces changes in the gut that create an environment hostile to parasites, 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 the gut wall, liver, lung and even central nervous system, inducing the formation of granulomas under the control of IL-13. 

IL-13 may antagonize Th1 responses that are required to resolve intracellular infections. 

Dysregulated IL-13 is 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 mild asthma after allergen challenge.

Multiple polymorphisms of IL-13 and genes encoding the IL-13 receptors as associated with asthma susceptibility, bronchial hyperresponsiveness, and increased IgE levels.

IL-13 over expression induces many features of allergic lung disease, including airway hyperresponsiveness, goblet cell metaplasia, mucus hypersecretion and airway remodelling which all contribute to airway obstruction.

IL-13 is overexpressed in sputum, bronchial submucosa, peripheral blood and mast cells in the airway smooth muscle bundle.

IL-13 induces secretion of chemokines that are required for recruitment of allergic effector cells to the lung. 

Polymorphisms in the IL-13 gene have been shown to confer an enhanced risk of atopic respiratory diseases such as asthma.

Research suggests that IL-13 is responsible for the promotion of the survival and the migration of epithelial cells, production of nitric oxide synthase by airway epithelial cells, activation of macrophages, permeability of the epithelial cells, and transformation of airway fibroblasts to myofibroblasts leading to collagen deposition, and  airway remodelling in asthmatic patients.

IL-13 suppresses proinflammatory mediators and it is involved in wound repair after injury.

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.

Dupilumab may be an effective form of treatment for asthmatic patients.

Cendakimab is also a monoclonal antibody to the IL-13 receptor.

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