Human IL-13 ELISA Development Kit

Name: Human IL-13 ELISA Development Kit
SKU: DEIA129
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

TBD

Species Reactivity

Human

Detection Method

sELISA

Intended Use

Human IL-13 ELISA Development Kit contains the key components required for the quantitative measurement of natural and/or recombinant IL-13 in a sandwich ELISA format. Using the ELISA protocol described below, this kit provides sufficient reagents to assay IL-13 in approximately 1500 ELISA plate wells.

Contents of Kit

1. Capture Antibody
2. Detection Antibody
3. Standard
4. StreptAvidin-HRP
5. TMB Liquid Substrate "Ready to Use"

Storage

See "Reagent Preparation"

General Description

Interleukin 13 (IL-13) is a cytokine secreted by many cell types, but especially T helper type 2 (Th2) cells¹, that is an important mediator of allergic inflammation and disease. 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 The functions of IL-13 overlap considerably with those of IL-4. Although IL-13 is associated primarily with the induction of airway disease, it also has anti-inflammatory properties. IL-13 induces many features of allergic lung disease, including airway hyperresponsiveness, goblet cell metaplasia and mucus hypersecretion, which all contribute to airway obstruction.

Standard Curve

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Interleukin 12B rs3212227 T > G polymorphism was associated with an increased risk of gastric cardiac adenocarcinoma in a Chinese population

DISEASES OF THE ESOPHAGUS

Authors: Yin, J.; Wang, X.; Wei, J.; Wang, L.; Shi, Y.; Zheng, L.; Tang, W.; Ding, G.; Liu, C.; Liu, R.; Chen, S.; Xu, Z.; Gu, H.

Abstract

Gastric cardiac adenocarcinoma (GCA) is one of common malignant tumors in the world. Multiple genes that play critical roles in inflammatory pathways probably are associated with GCA risk. We conducted a hospital-based case-control study to evaluate the genetic effects of functional single nucleotide polymorphisms (SNPs): interleukin 9 (IL9) rs31563 C>T, IL9 rs31564 G>T, IL10 rs1800872 T>G, IL12A rs2243115 T>G, IL12B rs3212227 T>G, and IL13 rs1800925 C>T on the development of GCA. Two hundred and forty-three GCA cases and 476 controls were recruited. Their genotypes were determined using a custom-by-design 48-Plex SNPscan kit. IL12B rs3212227 T>G polymorphism was associated with the increased risk of GCA. However, there was no significant association between the other five SNPs and GCA risk. Stratified analyses indicated that the risk of GCA associated with the IL12B rs3212227 T>G polymorphism was evident among female patients and patients who never smoked or consumed alcoholic drinks. These findings indicated that functional polymorphism IL12B rs3212227 T>G might correlate with GCA risk. However, our results were obtained with a limited sample size; the power of our analysis was low. Larger studies are required to confirm the current findings.

IL-1 beta prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early-life rhinovirus infection in mice

ALLERGY

Authors: Han, Mingyuan; Ishikawa, Tomoko; Bermick, Jennifer R.; Rajput, Charu; Lei, Jing; Goldsmith, Adam M.; Jarman, Caitlin R.; Lee, Julie; Bentley, J. Kelley; Hershenson, Marc B.

Abstract

Background: Early-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33. We examined regulation of this asthma-like phenotype by IL-1 beta. Methods: Six-day-old wild-type or NRLP3-/- mice were inoculated with sham or RVA1B. Selected mice were treated with IL-1 receptor antagonist (IL-1RA), anti-IL-1 beta, or recombinant IL-1 beta. Results: Rhinovirus infection induced Il25, Il33, Il4, Il5, Il13, muc5ac, and gob5 mRNA expression, ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness. RV also induced lung mRNA and protein expression of pro-IL-1 beta and NLRP3 as well as cleavage of caspase-1 and pro-IL-1 beta, indicating inflammasome priming and activation. Lung macrophages were a major source of IL-1 beta. Inhibition of IL-1 beta signaling with IL-1RA, anti-IL-1 beta, or NLRP3 KO increased RV-induced type 2 cytokine immune responses, ILC2 number, and mucus metaplasia, while decreasing IL-17 mRNA expression. Treatment with IL-1 beta had the opposite effect, decreasing IL-25, IL-33, and mucous metaplasia while increasing IL-17 expression. IL-1 beta and IL-17 each suppressed Il25, Il33, and muc5ac mRNA expression in cultured airway epithelial cells. Finally, RVinfected 6-day-old mice showed reduced IL-1 beta mRNA and protein expression compared to mature mice. Conclusion: Macrophage IL-1 beta limits type 2 inflammation and mucous metaplasia following RV infection by suppressing epithelial cell innate cytokine expression. Reduced IL-1 beta production in immature animals provides a mechanism permitting asthma development after early-life viral infection.