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・ Interlenghi
・ Interleukin
・ Interleukin 1 family
・ Interleukin 1 receptor antagonist
・ Interleukin 1 receptor, type I
・ Interleukin 1 receptor, type II
・ Interleukin 10
・ Interleukin 10 receptor, alpha subunit
・ Interleukin 10 receptor, beta subunit
・ Interleukin 11
・ Interleukin 11 receptor alpha subunit
・ Interleukin 12
・ Interleukin 12 receptor, beta 1 subunit
・ Interleukin 12 receptor, beta 2 subunit
・ Interleukin 12 subunit beta
Interleukin 13
・ Interleukin 13 receptor, alpha 1
・ Interleukin 15
・ Interleukin 15 receptor, alpha subunit
・ Interleukin 16
・ Interleukin 17
・ Interleukin 18
・ Interleukin 19
・ Interleukin 2
・ Interleukin 20
・ Interleukin 20 receptor, alpha subunit
・ Interleukin 20 receptor, beta subunit
・ Interleukin 21
・ Interleukin 22
・ Interleukin 23


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Interleukin 13 : ウィキペディア英語版
Interleukin 13

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 1.4kb. IL-13 and IL-4 exhibit a 30% of sequence similarity and have a similar structure. 〔 IL-13 is cytokine secreted by many cell types, but especially T helper type 2 (Th2) cells, that is a mediator of allergic 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 anti-inflammatory properties. IL-13 induces a class of protein-degrading enzymes, known as matrix metalloproteinases (MMPs), in the airways. These 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.
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 immunoglobulin E (IgE) secretion from activated human 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 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 transcription factor, signal transducer and activator of transcription 6 (STAT6). This can be resulted from an allergic reaction brought about when facing an Ala gene.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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