Il-13 is another th2 cytokine that is involved in asthma, and binds to theα chain of the il-4 receptor until recently, it was not possible to dissect the individual roles of il-4 and il-13 because of their similarity. Although il-4 and 5 play important roles in asthmatic inflammation, only il-13 will be discussed in this paper il-13 is released by both the innate and adaptive immune cells it can act on smooth muscles, alveolar macrophages, and may contribute to production of reactive oxygen species (ros) (de boever et al, 2014, p 1 woodruff et al, 2009, p 388. The effects of il-13 on immune cells are similar to those of il-4 as these cytokines share a common receptor subunit (the α subunit), although il-13 plays a predominant role in allergic inflammation by promoting bronchial hyperreactivity and overproduction of mucus. In light of recent developments, this review will explore our current understanding of the role of il-13 in the pathogenesis of allergy and asthma with a particular focus on new insights into the mechanisms by which il-13 induces the features of asthma.
In th2 cytokines, such as il-4, il-13 and il-5, which are important for ige synthesis and eosi- about vitamin d, and its known and potential role in asthma. T1 - role of periostin, feno, il-13, lebrikzumab, other il-13 antagonist and dual il-4/il-13 antagonist in asthma au - agrawal,swati au - townley,robert g py - 2014/2 y1 - 2014/2 n2 - introduction: asthma markedly diminishes quality of life due to limited activity, absences from work or school and hospitalizations. Ige antibodies play a crucial role in allergic type i reactions only il-4 and il-13 are able to induce an immunoglobulin isotype switch to ige in b cells a major question is to what extent these.
In cultures of purified t and b cells from allergic asthma patients and non-atopic controls, t cells were polyclonally stimulated to obtain il-4, il-13 and subsequently ige secretion the absolute amount of ige produced was not significantly different between patients and controls. Asthma is a reversible airway disease characterized by airway hyper-reactivity, inflammation and airway remodeling, and interleukin-13 (il-13) is a recognized effector in these processes for example, in a mouse model of asthma, il-13 signaling results in mucin secretion, airway hyper-reactivity, fibrosis, and chitinase up-regulation. As the role of il-13 in asthma has become more defined, a number of potential biomarkers for th2 airway inflammation, and hence il-13 activity, have been identified, including blood and sputum eosinophils, total serum ige, proteins derived from the bronchial epithelium (eg, serum periostin), and exhaled nitric oxide. This is a concise review on interleukin (il)-13 and the evolution of asthma therapy, from discovery of the molecule, the identification of its pathogenic role in animal models of asthma, to the development of clinically successful neutralizing agents.
The recent development of monoclonal antibodies directed against il-13 is now providing clinical investigators with opportunities to better define the relevant effects of il-13 in asthma and to determine whether il-13 inhibition is effective in patients refractory to existing therapies. Abstract asthma is a chronic inflammatory disease of the lower airways characterised by intermittent airway narrowing and airflow obstruction the aim of this study was to examine the association of il-13 arg 130 gln (a/g) and -1112c/t cytokine gene polymorphisms and to know the secretion of il-13 cytokine levels and the interactions between the il-13 130a/g and il-13rα1/il-4rα complex. Interleukin 13 (il-13) is a protein that in humans is encoded by the il13 gene il-13 was first cloned in 1993 and is located on chromosome 5q31 with a length of 14kb it has a mass of 13 kda and folds into 4 alpha helical bundles.
This suggests that il-13 plays an important role in corticosteroid resistant asthma and suggests that il-13 antagonist should be beneficial in corticosteroid resistant asthma grunig g, warnock m, wakil ae, et al requirement for il-13 independently of il-4 in experimental asthma. In particular, the symptoms of asthma are closely associated with the presence of activated t-helper 2 cell (th2) cytokine-producing cells [interleukin (il)-4, il-5, il-9, and il-13] in the airway wall. Il-13 role in mucus production goblet cell hyperplasia and mucus overproduction are features of asthma and chronic obstructive pulmonary disease and can lead to airway plugging, a pathologic feature of fatal asthma [21-23] animal models demonstrate that il-13 induces goblet cell hyperplasia and mucus hypersecretion [24,25.
Il-13 has many actions similar to those of il-4 and also regulates ige production but, unlike il-4, it does not regulate t cell differentiation to th2 cells and t lymphocytes do not respond to il-13 the role of il-13 in asthma was recently reviewed in this journal by marsha wills-carp [ 9 . Bronchial epithelium reconstituted in vitro from these subjects, on culture in air-liquid interface, was assayed for pigr expression and regulation by il-4/il-13 measurements and main results: downregulation of pigr protein was observed in the bronchial epithelium from patients with asthma ( p = 00002 vs control subjects. The cytokine il-13 is known to have a role in the pathogenesis of allergic asthma and thus is an important therapeutic target greater concentrations of this cytokine are observed in severe asthma and during exacerbations.
The development of a cd4 th2 immune response and its associated cytokines (eg il-4, il-5, and il-13) are known to play an important role in the pathogenesis of allergic asthma il-4 promotes ig isotype switching in b cells to produce primarily ige and igg1 ( 1 . Summary: this is a concise review on interleukin (il)-13 and the evolution of asthma therapy, from discovery of the molecule, the identification of its pathogenic role in animal models of asthma, to the development of clinically suc.
Il-13 levels in the sputum and bronchial biopsy samples remain elevated in severe asthma despite the use of inhaled and systemic corticosteroids thus, il-13 is a mediator involved in corticosteroid resistance. Interleukin-13 is a pleiotropic th2 cytokine that has been shown to be central to the pathogenesis of asthma some of the most prominent of the effects of il-13 include increases in goblet cell differentiation, activation of fibroblasts, elevation of bronchial hyperresponsiveness, and switching of b. Asthma has been linked to chromosome 5q31-33 through genome searches and screening of candidate genes [21, 22]this locus includes the genes for the t h 2 cytokines il-4, il-5, il-9, and il-13.