IL-17E, a Novel Proinflammatory Ligand for the IL-17 Receptor Homolog IL-17Rh1

Abstract

We report identification of interleukin (IL)-17E, a novel member of the IL-17 family of cytokines. IL-17E is a ligand for the recently identified protein termed EVI27/IL-17BR, which we term IL-17 receptor homolog 1 (IL-17Rh1) in light of the multiple reported ligand-receptor relationships. Murine EVI27 was identified through its location at a common site of retroviral integration in BXH2 murine myeloid leukemias. IL-17Rh1 shows highest level expression in kidney with moderate expression in multiple other organs, whereas IL-17E mRNA was detected at very low levels in several peripheral tissues. IL-17E induces activation of NF-B and stimulates production of the proinflammatory chemokine IL-8.

Low-Dose Peptide Tolerance Therapy of Lupus Generates Plasmacytoid Dendritic Cells That Cause Expansion of Autoantigen-Specific Regulatory T Cells and Contraction of Inflammatory Th17 Cells

“…Lowdose H4 71-94 tolerance also prevented infiltration of Th17 cells in kidney (Fig. 3F), but we could observe some linear staining in glomeruli from both control and peptide-tolerized mice, probably due to expression of IL-17Rs on kidney cells (45).…”

Exploring the two-gene ratio in breast cancer—independent roles for HOXB13 and IL17BR in prediction of clinical outcome

“…The protein is a cytokine receptor that specifically binds to IL17B and IL17E in the IL17 family [29,30]. One may speculate that IL17BR could act in a protective way by taking part in the immune response against cancer cells, but this remains to be shown.…”

Inhibitory Effect of Recombinant IL-25 on the Development of Dextran Sulfate Sodium-Induced Experimental Colitis in Mice

“…IL-25 is reported to be produced by Th2 and mast cells (8,9). IL-25 was also shown to induce production of pro-inflammatory chemokine IL-8 and to activate NF-B1 (10). Initially, treatment of mice with rIL-25 was shown to induce massive histological and pathological changes in the gastrointestinal (GI) tract (8).…”