Human IL-17RE Antibody Summary
Accession # Q8NFR9
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.
Detection of IL-17 RE in HEK293 Human Cell Line Transfected with Human IL-17 RE and eGFP by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with either (A) human IL-17 RE or (B) human IL-17 RA and eGFP was stained with Mouse Anti-Human IL-17 RE Monoclonal Antibody (Catalog # MAB8358) followed by Allophycocyanin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0101B). Quadrant markers were set based on control antibody staining (Catalog # MAB002). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
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 human IL-17 RE consists of a 431 amino acid (aa) extracellular domain, a 21 aa transmembrane segment, and a 192 aa cytoplasmic domain with one SEFIR/TIR domain (3). Within aa 115-454, human IL-17 RE shares 79% aa sequence identity with mouse and rat IL-17 RE. Alternative splicing of human IL-17 RE generates additional isoforms with a 116 aa N-terminal deletion and/or substitution and truncation in the ECD following aa 268 or aa 433. 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).
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- Pfeifer, P. et al. (2013) Am. J. Respir. Cell Mol. Biol. 48:415.
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- Yamaguchi, Y. et al. (2007) J. Immunol. 179:7128.
- Johansen, C. et al. (2009) Br. J. Dermatol. 160:319.
- Reynolds, J.M. et al. (2012) J. Immunol. 189:4226.
- Liao, R. et al. (2013) J. Exp. Clin. Cancer Res. 32:3.
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