IL13


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IL13

A gene on chromosome 5q31 that encodes interleukin-13, an immunoregulatory cytokine produced primarily by activated Th2 cells which is involved in B-cell maturation and differentiation. IL13 upregulates CD23 and MHC class II expression and promotes IgE isotype switching in B cells; it downregulates macrophage activity, inhibiting production of pro-inflammatory cytokines and chemokines.

Molecular pathology
IL-13 plays a central in the pathogenesis of allergen-induced asthma by IgE- and eosinophil-independent mechanisms.
References in periodicals archive ?
Group 1 producing IFN gamma, Group 2 producing IL5 and IL13, Group 3 producing IL17 and/or IL22.
In our research, we genotyped six SNP loci from the five candidate genes (IL13, IL4, IL4RA, MS4A2, ADRB2) in Mauritian Indian and Chinese Han populations in order to determine their association with asthma.
IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells.
Important susceptibility genes include the IL4 receptor alpha gene, IL4 gene, the IL13 gene, Stat 6 genes regulating IgE expression, Adam 33 and the HLA-G genes.
Malignant glioma cells, as compared to normal brain cells, express interleukin-13 (IL13) receptors at a high density.
IL13-PE38 uses the IL13 protein to target receptors on brain and kidney tumors, while SS1-PE38 uses the monoclonal antibody SS1(dsFv) to target receptors found in mesothelioma, ovarian cancer and other tumors.
It is thought certain people have the two molecules, known as IL-4 and IL13 in their lungs as part of their genetic make up.
The lack of responsiveness of fibroblasts to TRAIL might be due to the lack of TRAIL ligand (as a consequence of decreased expression and/or myeloid cell recruitment into the lungs, as revealed by decreased CD33 cells), internalization of the TRAIL receptors, and increased presence of IL13 or other intrinsic differences between IPF and normal lung fibroblasts.
The genetic variants of pro-inflammatory cytokines (IL4, IL13, IL10, IL18, TNF, and IFNGR1), the cytokine receptor (IL4R), the genes involved in the IgE/Fc[epsilon]RI pathway (the galectin-3 gene (LGALS3)), and nucleotide-binding oligomerization domain (NOD) gene polymorphisms are also strongly associated with betalactam-induced immediate reactions (Table 2) [67-73].
Herein, we assessed cytokines and growth factors crucial for eosinophil proliferation and differentiation (GM-CSF, IL5, and IL4), for their release from bone marrow (IL5), for their survival (IL5, IL13, GM-CSF, and IL4) and priming in circulation (IL5, GM-CSF, IL4, and TNF[alpha]), and for extravasation (IL4, IFN[gamma], TNF[alpha], IL8, and eotaxin) and homing into the gut (eotaxin, RANTES, IL5, IL8, IL13, GM-CSF, and TNF[alpha]) as well as responsible for inducing production and secretion of their mediators (TNF[alpha], IFN[gamma], IL-5, GM-CSF, and eotaxin) (reviewed in [10, 17, 20]).
AD has a complex etiology that involves activation of multiple immunological and inflammatory pathways along with disruption of epidermal barriers, elevated IgE levels, peripheral eosinophilia, and a predominance of Th2 cells expressing IL-4, IL-5, and IL13 [2].