IL17 Mouse ELISA Kit

Name: IL17 Mouse ELISA Kit
SKU: DEIA1519
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

serum, plasma, cell culture supernatants

Species Reactivity

Mouse

Detection Method

sELISA

Intended Use

For the quantitative measurement of Mouse IL17 concentrations in serum, plasma and cell culture supernatants.

Contents of Kit

1. IL-17A Microplate (Item A), 96 wells (12 strips x 8 wells) coated with anti-Mouse IL-17A
2. Wash Buffer Concentrate (20×) (Item B), 25 ml of 20× concentrated solution.
3. Standard Protein (Item C), 2 vials of Mouse IL-17A. 1 vial is enough to run each standard in duplicate.
4. Detection Antibody IL-17A (Item F), 2 vials of biotinylated anti-Mouse IL-17A. Each vial is enough to assay half the microplate.
5. HRP-Streptavidin Concentrate (Item G), 200 μl 700× concentrated HRP-conjugated streptavidin.
6. TMB One-Step Substrate Reagent (Item H), 12 ml of 3,3,5,5'-tetramethylbenzidine (TMB) in buffer solution.
7. Stop Solution (Item I) 8 ml of 0.2 M sulfuric acid.
8. Assay Diluent A (Item D), 30 ml of diluent buffer, 0.09% sodium azide as preservative.
9. Assay Diluent B (Item E), 15 ml of 5× concentrated buffer.

Storage

The entire kit may be stored at -20°C for up to 1 year from the date of shipment. Avoid repeated freeze-thaw cycles. The kit may be stored at 4°C for up to 6 months. For extended storage, it is recommended to store at -80°C. For prepared reagent storage, see table below.

Precision

Intra-Assay CV%: <10%
Inter-Assay CV%: <12%

Sensitivity

The minimum detectable dose of Mouse IL-17A was determined to be 6 pg/ml. Minimum detectable dose is defined as the analyte concentration resulting in an absorbance that is 2 standard deviations higher than that of the blank (diluent buffer).

General Description

The protein encoded by this gene is a proinflammatory cytokine produced by activated T cells. This cytokine regulates the activities of NF-kappaB and mitogen-activated protein kinases. This cytokine can stimulate the expression of IL6 and cyclooxygenase-2 (PTGS2/COX-2), as well as enhance the production of nitric oxide (NO). High levels of this cytokine are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis and multiple sclerosis.

Standard Curve

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Investigation of the role of IL17A gene variants in Chagas disease

GENES AND IMMUNITY

Authors: Leon Rodriguez, D. A.; Echeverria, L. E.; Gonzalez, C. I.; Martin, J.

Abstract

Human host genetic factors have been suggested to be determinants of the prevalence and clinical forms of Chagas disease. In this regard, IL-17A is believed to control parasitemia and protect against heart disease. In this work, we assessed whether IL17A gene polymorphisms are related to infection and/or development of the cardiac form of Chagas disease by genotyping for five IL17A SNPs (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) in 1171 individuals from a Colombian region endemic for Chagas disease, classified as seronegative (n = 595), seropositive asymptomatic (n = 175) and chronic Chagas cardiomyopathy (n = 401). Our results showed that SNP rs8193036, which is located upstream of the coding region of the gene, was slightly associated with protection against T. cruzi infection (P = 0.0170, P-FDR = 0.0851, odds ratio (OR) = 0.80, confidence interval (CI) = 0.66-0.96) and associated with protection against the development of cardiomyopathy (P = 0.0065, P-FDR = 0.0324, OR = 0.75, CI = 0.60-0.92). This finding suggests that this IL17A polymorphism could be associated with Trypanosoma cruzi infection and the development of chronic cardiomyopathy due to differential expression of cytokine IL-17A.

Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts

SCIENCE TRANSLATIONAL MEDICINE

Authors: Uluckan, Oezge; Jimenez, Maria; Karbach, Susanne; Jeschke, Anke; Grana, Osvaldo; Keller, Johannes; Busse, Bjoern; Croxford, Andrew L.; Finzel, Stephanie; Koenders, Marije; van den Berg, Wim; Schinke, Thorsten; Amling, Michael; Waisman, Ari; Schett, Georg; Wagner, Erwin F.

Abstract

Inflammation has important roles in tissue regeneration, autoimmunity, and cancer. Different inflammatory stimuli can lead to bone loss by mechanisms that are not well understood. We show that skin inflammation induces bone loss in mice and humans. In psoriasis, one of the prototypic IL-17A-mediated inflammatory human skin diseases, low bone formation and bone loss correlated with increased serum IL-17A levels. Similarly, in two mouse models with chronic IL-17A-mediated skin inflammation, K14-IL17A(ind) and JunB(Delta ep), strong inhibition of bone formation was observed, different from classical inflammatory bone loss where osteoclast activation leads to bone degradation. We show that under inflammatory conditions, skin-resident cells such as keratinocytes, gamma delta T cells, and innate lymphoid cells were able to express IL-17A, which acted systemically to inhibit osteoblast and osteocyte function by a mechanism involving Wnt signaling. IL-17A led to decreased Wnt signaling in vitro, and importantly, pharmacological blockade of IL-17A rescued Wnt target gene expression and bone formation in vivo. These data provide a mechanism where IL-17A affects bone formation by regulating Wnt signaling in osteoblasts and osteocytes. This study suggests that using IL-17A blocking agents in psoriasis could be beneficial against bone loss in these patients.