IL17AF ELISA Kit

Name: IL17AF ELISA Kit
SKU: DEIA3730
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Cell Culture Supernatant

Species Reactivity

Human

Detection Method

sELISA

Intended Use

IL17AF ELISA Kit is a sandwich enzyme immunoassay for the quantitative measurement of free IL17AF in the supernatant of activated cells.

Contents of Kit

1. 100× Capture Antibody (Contains 0.02% Sodium azide. Sodium azide is highly toxic.): 250 μL
2. 100× Detection Antibody (Contains 0.02% Sodium azide. Sodium azide is highly toxic.): 250 μL
3. BSA: 0.5 g × 4
4. 20× Wash Buffer: 50 mL
5. Coating Buffer: 25 mL
6. 10× Blocking Buffer: 20 mL
7. HRP-Conjugated Streptavidin: 10 μL
8. ABTS Substrate: 2 × 12 mL
9. Recombinant IL-17AF Standard: 1 vial
10. ELISA Strip 96 Well Plates: 96 well

Storage

Except Recombinant IL-17AF Standard stored at -20 °C, other reagents are stored at 4 °C.

Sensitivity

4000 pg/mL is a recommended starting dilution. By reducing the starting concentration, researchers can determine the lowest detection limit of IL-17AF protein in the test samples.

General Description

Interleukin 17 (IL-17) is a pro-inflammatory cytokine produced by a subset of T helper cells that develops distinct from the Th1- and Th2- cell differentiation pathways. IL-17, also known as CTLA-8, stimulates induction of other pro-inflammatory cytokines TNF alpha, IL-1 beta, IL-6, and IL-8, and reports strongly suggest the involvement of IL-17 in several chronic inflammatory diseases such as rheumatoid arthritis, psoriasis and multiple sclerosis. TGFβ (differentiation) and IL-23 (expansion) are required for induction and maintenance of Th17 (IL-17 producing) cells, which in turn induce the other proinflammatory cytokines. IL-17 (~32 kDa) protein is produced and exists as a homo-dimer, has homology to a herpes virus early protein, is one of the six members (IL-17A-F) of this cytokine family, and is well characterized and highly expressed by activated effector memory T cells.

Standard Curve

Following the provided protocol, human IL-17AF standard was titrated to determine detectible levels.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1

CELL REPORTS

Authors: Uluckan, Ozge; Jimenez, Maria; Roediger, Ben; Schnabl, Jakob; Diez-Cordova, Lucia T.; Troule, Kevin; Weninger, Wolfgang; Wagner, Erwin F.

Abstract

Atopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunB(Delta ep) mice, with a large transcriptomic overlap with AD. Additionally, using Rag1(-/-) mice, we demonstrate that adaptive immune cells are necessary for protection against S. aureus colonization. Prophylactic antibiotics, but not antibiotics after established dysbiosis, reduce IL-17A expression and skin inflammation, examined using Il17a-eGFP reporter mice. Mechanistically, keratinocytes lacking JunB exhibit higher MyD88 levels in vitro and in vivo, previously shown to regulate S. aureus colonization. In conclusion, our data identify JunB as an upstream regulator of microbiota-immune cell interactions and characterize the IL-17A response upon spontaneous dysbiosis.

IL-17A-mediated ERK1/2/p65 signaling pathway is associated with cell apoptosis after non-alcoholic steatohepatitis

IUBMB LIFE

Authors: Pan, Ya-jie; Ren, Xing; Zhang, Ying-ying; Lv, Jun; Zeng, Qing-lei; Zhang, Hong-yu; Yu, Zu-jiang

Abstract

Interleukin (IL)-17A is pro-inflammatory cytokine which has been identified as a noninvasive marker of the pathogenesis of non-alcoholic steatohepatitis (NASH). However, the underlying role of IL-17A in NASH progression remains unclear. This study was designed to investigate the biological function and molecular mechanism of IL-17A in the induction of NASH. The results showed that IL-17A was highly expressed in high-fat diet (HFD)-induced NASH mouse model. Intravenous injection of IL-17A exacerbated steatohepatitis process via promoting hepatocyte apoptosis. Furthermore, IL-17A-induced apoptosis was mediated by ERK1/2/p65 signaling pathway. In conclusion, we demonstrated that IL-17A-mediated ERK1/2/p65 signaling pathway was a promising target for the treatment of NASH. (c) 2018 IUBMB Life, 71(3):302-309, 2019