IL-17A ELISA Kits

Interleukin-17 (IL-17 or IL-17A) is the founding member of a group of cytokines called the IL-17 family. IL-17A was originally identified as a transcript from a rodent T-cell hybridoma by Rouvier et al. in 1993. Known as CTLA8 in rodents, IL-17 shows high homology to viral IL-17 encoded by an open reading frame of the T lymphotropic rhadinovirus Herpesvirus saimiri.[1] To elicit its functions, IL-17 binds to a type I cell surface receptor called IL-17R of which there are at least three variants IL17RA, IL17RB, and IL17RC.[2] In addition to IL-17A, members of the IL-17 family include IL-17B, IL-17C, IL-17D, IL-17E (also called IL-25), and IL-17F. All members of the IL-17 family have a similar protein structure, with four highly conserved cysteine residues critical to their 3-dimensional shape, yet they have no sequence similarity to any other known cytokines.

The most notable role of IL-17 is it involvement in inducing and mediating proinflammatory responses. IL-17 is commonly associated with allergic responses. IL-17 induces the production of many other cytokines (such as IL-6, G-CSF, GM-CSF, IL-1β, TGF-β, TNF-α), chemokines (including IL-8, GRO-α, and MCP-1), and prostaglandins (e.g., PGE2) from many cell types (fibroblasts, endothelial cells, epithelial cells, keratinocytes, and macrophages). The release of cytokines causes many functions, such as airway remodeling, a characteristic of IL-17 responses. The increased expression of chemokines attracts other cells including neutrophils but not eosinophils. IL-17 function is also essential to a subset of CD4+ T-Cells called T helper 17 (Th17) cells. As a result of these roles, the IL-17 family has been linked to many immune/autoimmune related diseases including rheumatoid arthritis, asthma, lupus, allograft rejection and anti-tumour immunity.[3]

Much progress has been made in the understanding of the regulation of IL-17. At first, Aggarwal et al. showed that production of IL-17 was dependent on IL-23.[4] Later, a Korean group discovered that STAT3 and NF-κB signalling pathways are required for this IL-23-mediated IL-17 production.[5] Consistent with this finding, Chen et al. showed that another molecule, SOCS3, plays an important role in IL-17 production.[6] In the absence of SOCS3, IL-23-induced STAT3 phosphorylation is enhanced, and phosphorylated STAT3 binds to the promotor regions of both IL-17A and IL-17F increasing their gene activity. In contrast, some scientists believe IL-17 induction is independent of IL-23. Several groups have identified ways to induce IL-17 production both in vitro[7] and in vivo[8][9] by distinct cytokines, called TGF-β and IL-6, without the need for IL-23.[7][8][9] Although IL-23 is not required for IL-17 expression in this situation, IL-23 may play a role in promoting survival and/or proliferation of the IL-17 producing T-cells. Recently, Ivanov et al. found that the thymus specific nuclear receptor, ROR-γ, directs differentiation of IL-17-producing T cells.[10]

Pig IL-17A ELISA  Catalog No. E101-807

Bovine IL-17A ELISA  Catalog No. E11-806

References
1. Rouvier E, Luciani MF, Mattéi MG, Denizot F, Golstein P (1993). "CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instability sequences, and homologous to a herpesvirus saimiri gene". J. Immunol. 150 (12): 5445–56.

2. Starnes T, Broxmeyer HE, Robertson MJ, Hromas R (2002). "Cutting edge: IL-17D, a novel member of the IL-17 family, stimulates cytokine production and inhibits hemopoiesis". J. Immunol. 169 (2): 642–6.

3. Aggarwal S, Gurney AL (2002). "IL-17: prototype member of an emerging cytokine family". J. Leukoc. Biol. 71 (1): 1–8.

4. Aggarwal S, Ghilardi N, Xie MH, de Sauvage FJ, Gurney AL (2003). "Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17". J. Biol. Chem. 278 (3): 1910–4.

5. Cho ML, Kang JW, Moon YM, Nam HJ, Jhun JY, Heo SB, Jin HT, Min SY, Ju JH, Park KS, Cho YG, Yoon CH, Park SH, Sung YC, Kim HY (2006). "STAT3 and NF-kappaB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice". J. Immunol. 176 (9): 5652–61.

6. Chen Z, Laurence A, Kanno Y, Pacher-Zavisin M, Zhu BM, Tato C, Yoshimura A, Hennighausen L, O'Shea JJ (2006). "Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells". Proc. Natl. Acad. Sci. U.S.A. 103 (21): 8137–42.

7. Veldhoen M, Hocking RJ, Atkins CJ, Locksley RM, Stockinger B (2006). "TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells". Immunity 24 (2): 179–89.

8. Mangan PR, Harrington LE, O'Quinn DB, Helms WS, Bullard DC, Elson CO, Hatton RD, Wahl SM, Schoeb TR, Weaver CT (2006). "Transforming growth factor-beta induces development of the T(H)17 lineage". Nature 441 (7090): 231–4.

9. Bettelli E, Carrier Y, Gao W, Korn T, Strom TB, Oukka M, Weiner HL, Kuchroo VK (2006). "Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells". Nature 441 (7090): 235–8.

10. Ivanov, II, B.S. McKenzie, L. Zhou, C.E. Tadokoro, A. Lepelley, J.J. Lafaille, D.J. Cua, and D.R. Littman. 2006. The orphan nuclear receptor ROR-γ directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell 126:1121-1133.