Mouse IL-17RE Alexa Fluor® 488-conjugated Antibody

Applications

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Preparation and Storage

Background: IL-17RE

Interleukin‑17 Receptor E (IL‑17 RE) is an approximately 70 kDa (predicted) transmembrane protein in the family of IL‑17 receptors. IL‑17 RE is required for mediating the pro‑inflammatory and homeostatic actions of IL‑17C in the skin and mucosa (1, 2). Mature mouse IL‑17 RE consists of a 391 amino acid (aa) extracellular domain, a 21 aa transmembrane segment, and a 202 aa cytoplasmic domain with one SEFIR/TIR domain (3). Within aa 115‑414, mouse IL‑17 RE shares 79% and 90% aa sequence identity with human and rat IL‑17 RE, respectively. Alternative splicing of mouse IL‑17 RE generates additional isoforms with either 201 aa or 326 aa
N‑terminal deletions or deletion/substitution of the transmembrane segment (3). IL‑17 RE is expressed on keratinocytes, mucosal epithelial cells, Th17 cells, and gamma /δ T cells (4, 5). It associates with the widely expressed IL‑17 RA to form a heterodimeric receptor for IL-17C (4‑6). IL-17C binds to IL‑17 RE with high affinity and to
IL‑17 RA with low affinity (4, 5). IL‑17C expression is induced by inflammatory stimulation in colon and airway epithelial cells, keratinocytes, CD4⁺ T cells, macrophages, and dendritic cells (4, 6, 7‑9). It is up‑regulated in various chronic inflammatory diseases including psoriasis, cystic fibrosis, and chronic obstructive pulmonary disease (COPD) (7, 8, 10). IL‑17 RE is reciprocally down‑regulated in psoriatic lesions (10). The interaction of IL‑17C with IL‑17 RE promotes mucosal immunity through the induction of anti‑bacterial peptides and pro‑inflammatory cytokines and chemokines (4, 6, 8, 9). IL‑17C action supports the integrity of the colon epithelium following infection induced damage (4, 6, 11) but also contributes to psoriatic skin thickening and the progression of arthritis (4, 8, 9). IL‑17C is additionally up‑regulated in Th17 cell dependent autoimmunity (5). In this setting, it exacerbates disease severity by inducing Th17 cell production of IL‑17A, IL‑17F, IL‑22, CCR6, and CCL20 (5). The up‑regulation of IL‑17 RE in hepatocellular carcinoma is associated with poor prognosis (12).

Product Datasheets

Product Specific Notices

This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.

Related Research Areas

• IL-17 Family