Interleukin 13
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
| Interleukin 13
| ||||||||||||||
| Image:PBB Protein IL13 image.jpg | ||||||||||||||
| PDB rendering based on 1ga3. | ||||||||||||||
| Identifiers | ||||||||||||||
| Symbol(s) | IL13; ALRH; BHR1; IL-13; MGC116786; MGC116788; MGC116789; P600 | |||||||||||||
| External IDs | OMIM: 147683 MGI: 96541 Homologene: 1649 | |||||||||||||
| ||||||||||||||
| RNA expression pattern | ||||||||||||||
| Orthologs | ||||||||||||||
| Human | Mouse | |||||||||||||
| Entrez | 3596 | 16163 | ||||||||||||
| Ensembl | ENSG00000169194 | ENSMUSG00000020383 | ||||||||||||
| Uniprot | P35225 | Q5SUZ9 | ||||||||||||
| Refseq | NM_002188 (mRNA) NP_002179 (protein) | NM_008355 (mRNA) NP_032381 (protein) | ||||||||||||
| Location | Chr 5: 132.02 - 132.02 Mb | Chr 11: 53.47 - 53.48 Mb | ||||||||||||
| Pubmed search | [1] | [2] | ||||||||||||
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview
Interleukin 13 (IL-13) is a cytokine secreted by many cell types, but especially T helper type 2 (Th2) cells[1], that is an important mediator of allergic inflammation and disease.
Functions
In addition to effects on immune cells that are similar to those of the closely related cytokine IL-4, IL-13 is more importantly implicated as a central mediator of the physiologic changes induced by allergic inflammation in many tissues. IL-13 induces its effects through a multi-subunit receptor that includes the alpha chain of the IL-4 receptor (IL-4Rα), which is also a component of the IL-4 receptor, and at least one of two known IL-13-specific binding chains[1]. 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).
The functions of IL-13 overlap considerably with those of IL-4, especially with regard to changes induced on hematopoietic cells, but these effects are probably less important given the more potent role of IL-4. Thus, although IL-13 can induce immunoglobulin E (IgE) secretion from activated human B cells, deletion of IL-13 from mice does not markedly affect either Th2 cell development or antigen-specific IgE responses induced by potent 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.
Although IL-13 is associated primarily with the induction of airway disease, it also has anti-inflammatory properties. Airway matrix metalloproteinases (MMPs), which are protein-degrading enzymes, are required to induce egression of effete 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.
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 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 induces many features of allergic lung disease, including airway hyperresponsiveness, goblet cell metaplasia and mucus hypersecretion, which all contribute to airway obstruction [1]. IL-4 contributes to these physiologic changes, but is less important than IL-13. IL-13 also induces secretion of 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 asthma.
See also
IL-13R, the IL-13 receptor
References
Further reading
- Marone G, Florio G, Petraroli A, de Paulis A (2001). "Dysregulation of the IgE/Fc epsilon RI network in HIV-1 infection.". J. Allergy Clin. Immunol. 107 (1): 22-30. PMID 11149986.
- Marone G, Florio G, Triggiani M, et al. (2001). "Mechanisms of IgE elevation in HIV-1 infection.". Crit. Rev. Immunol. 20 (6): 477-96. PMID 11396683.
- Skinnider BF, Kapp U, Mak TW (2003). "The role of interleukin 13 in classical Hodgkin lymphoma.". Leuk. Lymphoma 43 (6): 1203-10. PMID 12152987.
- Izuhara K, Arima K, Yasunaga S (2003). "IL-4 and IL-13: their pathological roles in allergic diseases and their potential in developing new therapies.". Current drug targets. Inflammation and allergy 1 (3): 263-9. PMID 14561191.
- Dessein A, Kouriba B, Eboumbou C, et al. (2005). "Interleukin-13 in the skin and interferon-gamma in the liver are key players in immune protection in human schistosomiasis.". Immunol. Rev. 201: 180-90. doi:10.1111/j.0105-2896.2004.00195.x. PMID 15361241.
- Copeland KF (2006). "Modulation of HIV-1 transcription by cytokines and chemokines.". Mini reviews in medicinal chemistry 5 (12): 1093-101. PMID 16375755.
Cytokines: interleukins | |
|---|---|
| IL-1 superfamily | IL-1 (IL-1Ra) - IL-18 - IL-33 |
| IL-6 like/gp130 utilizing | IL-6 - IL-11 - IL-27 - IL-30 - IL-31 |
| IL-10 family | IL-10 - IL-19 - IL-20 - IL-22 - IL-24 - IL-26 |
| Interferon type III | IL-28 - IL-29 |
| Common γ-chain family | IL-2/IL-15 - IL-3 - IL-4 - IL-7 - IL-9 - IL-13 - IL-21 |
| IL-12 family | IL-12 - IL-23 - IL-27 - IL-35 |
| Other | IL-5 - IL-8 - IL-14 - IL-16 - IL-17/IL-25 (A) - IL-32 |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
