IL-18 receptors, their role in ligand binding and function: Anti-IL-1RAcPL antibody, a potent antagonist of IL-18
Journal of Immunology, ISSN: 0022-1767, Vol: 165, Issue: 9, Page: 4950-4956
2000
- 72Citations
- 47Captures
- 2Mentions
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Metrics Details
- Citations72
- Citation Indexes72
- 72
- CrossRef68
- Captures47
- Readers47
- 47
- Mentions2
- References2
- Wikipedia2
Article Description
IL-18 is critical in eliciting IFN-γ production from Th1 cells both in vitro and in vivo. Th1 cells have been implicated in the pathogenesis of autoimmune disorders, making antagonists of IL-18 promising therapeutics, However, specificity and binding characteristics of IL-18R components have only been superficially explored. In this study, we show that IL-1R related protein 1 (IL-1Rrp1) and IL-1R accessory protein-like (IL-1RAcPL) confer responsiveness to IL-18 in a highly specific (no response to other IL-1 ligands) and unique manner (no functional pairing with other IL-1Rs and IL-1R-like molecules). Cotransfection with both receptor components resulted in expression of both low and high affinity binding sites for IL-18 (K(d) of 11 and 0.4 nM, respectively). We prepared anti-IL-1RAcPL mAb TC30-28E3, which, in contrast to soluble R proteins, effectively inhibited the IL-18-induced activation of NF-κB. Quantitative PCR showed that Th1 but not Th2 cells are unique in that they coexpress IL-1Rrp1 and IL-1RAcPL. mAb TC30-28E3 inhibited IL-18-induced production of IFN-γ by Th1 cells, being at least 10-fold more potent than anti-IL-18 ligand mAb. This study shows that IL-1RAcPL is highly specific to IL-18, is required for high affinity binding of IL-18, and that the anti-IL-1RAcPL mAb TC30-28E3 potently antagonizes IL-18 responses in vitro, providing a rationale for the use of anti-IL-1RAcPL Abs to inhibit Th1-mediated inflammatory pathologies.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034326652&origin=inward; http://dx.doi.org/10.4049/jimmunol.165.9.4950; http://www.ncbi.nlm.nih.gov/pubmed/11046021; https://journals.aai.org/jimmunol/article/165/9/4950/69891/IL-18-Receptors-Their-Role-in-Ligand-Binding-and; https://dx.doi.org/10.4049/jimmunol.165.9.4950; https://www.jimmunol.org/content/165/9/4950
Oxford University Press (OUP)
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