• Purity

  >95%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.01 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its ability to inhibit IL-17-induced IL-6 secretion by NIH‑3T3 mouse embryonic fibroblast cells. The ED    ₅₀ for this effect is 0.015-0.075 µg/mL in the presence of 10 ng/mL of recombinant mouse IL-17.

• Source

  Mouse myeloma cell line, NS0-derived

  Mouse IL-17 RA/IL-17 R (Ser32-Trp322) Accession # Q60943	IEGRMDP	Mouse IgG2A (Glu98-Lys330)
  N-terminus		C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Ser32

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  60.4 kDa (monomer)

• SDS-PAGE

  80-95 kDa, reducing conditions

Background: IL-17 RA/IL-17 R

IL-17 R, also known as IL-17 RA, is a 120 kDa type I transmembrane glycoprotein protein that plays a central role in inflammatory responses (1-3). Mature mouse IL‑17 R consists of a 291 amino acid (aa) extracellular domain, a 21 aa transmembrane segment, and a 521 aa cytoplasmic domain (4). The cytoplasmic domain contains a region homologous to the TIR domain of the TLR/IL-1 R family (5). Mouse IL-17 R shares 84% and 72% aa sequence identity with rat and human IL-17 R, respectively. Within the extracellular domain, it shares 18%-25  % sequence identity with mouse IL-17 RB, C, D, and E. While the expression of IL-17 is restricted to activated T cells, IL-17 R exhibits a broad tissue distribution (4). Even in the absence of ligand, IL-17 R exists on the cell surface as a multimer (6). IL-17 R can bind IL-17 but must associate with IL-17 RC to transduce signals (7, 8). Interestingly, human IL-17 R does not appear to form productive complexes with mouse IL-17 RC (8). The IL-17 R can also signal in response to IL-17F (9). IL-17 R ligation promotes T cell activation and the production of IL-6, G-CSF, SCF, and multiple pro‑inflammatory chemokines (4, 7, 9, 10). IL-17A and IL-17F synergize with TNF-alpha in the induction of CXCL1, G-CSF, and IL-6 (9, 11). This effect requires the presence of both TNF RI and TNF RII (9). IL-17 interactions with IL-17 R also inhibit the TNF-alpha induced up-regulation of fibroblast CCL5 and VCAM-1 (11). CCL5 and VCAM-1 induced effects are differentially sensitive to blockade with IL-17 R specific antibodies, suggesting that IL-17 R triggers divergent intracellular signals (11).   In vivo, IL‑17 R activity is important for increased generation of neutrophils and their recruitment to sites of inflammation (10, 12, 13). IL-17 R is required for host defense against microbial infection and for the progression of arthritis from inflammation to destructive joint erosion (10, 13).

• References:

1. Iwakura, Y. and H. Ishigame (2006) J. Clin. Invest. 116:1218.

2. Moseley, T.A. et al. (2003) Cytokine Growth Factor Rev. 14:155.

3. Kawaguchi, M. et al. (2004) J. Allergy Clin. Immunol. 114:1265.

4. Yao, Z. et al. (1995) Immunity 3:811.

5. Novatchkova, M. et al. (2003) Trends Biochem. Sci. 28:226.

6. Kramer, J.M. et al. (2006) J. Immunol. 176:711.

7. Hymowitz, S.G. et al. (2001) EMBO J. 20:5332.

8. Toy, D. et al. (2006) J. Immunol. 177:36.

9. McAllister, F. et al. (2005) J. Immunol. 175:404.

10. Ye, P. et al. (2001) J. Exp. Med. 194:519.

11. Schnyder, B. et al. (2005) Cytokine 31:191.

12. Tan, W. et al. (2006) J. Immunol. 176:6186.

13. Lubberts, E. et al. (2005) J. Immunol. 175:3360.

• Long Name:

  Interleukin 17 Receptor

• Entrez Gene IDs:

  23765 (Human); 16172 (Mouse); 312679 (Rat)

• Alternate Names:

  CD217 antigen; CD217; Cdw217; CDw217interleukin 17 receptor; hIL-17R; IL-17 R; IL-17 RA; IL-17 receptor A; IL17RA; IL-17RA; IL-17RAMGC10262; IL17Rinterleukin-17 receptor A; interleukin 17 receptor A