The interleukin-23 (IL-23) pathway, Th17 cells and gammadelta T cells which respond to IL-23 play major pro-inflammatory roles. We have used unique interleukin-23 receptor (IL-23R) subunit-specific monoclonal antibodies (mAb), X67 and X68, and interleukin-12 receptor beta-1 subunit (IL-12Rbeta1) expression levels to evaluate the IL-23R complex on CD4 alphabeta TCR T helper 17 (Th17) cells and on gammadelta T cells. Both IL-23R and IL-12Rbeta1 subunits constitute the functional IL-23R. Expression of the IL-23R subunit by cultured Th17 cells was heterogeneous. Th17 cells expressed consistent high levels of the IL-12Rbeta1 subunit, which appeared a better predictor of responsiveness to IL-23 than expression of the IL-23R subunit. Moreover, sorting memory CD4 T cells by high IL-12Rbeta1 expression selectively enriched cells committed to IL-17 production from the blood. IL-23R expression was also observed on freshly isolated and cultured gammadelta T cells and the cultured gammadelta T cells were not responsive to IL-23.Immunology and Cell Biology accepted article preview online, 20 September 2016.
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This work was funded by National Health and Research Council project grants and
the Cooperative Research Centre for Biomarker Translation and the Victorian
Operational Infrastructure Scheme. KK was supported by Arthritis Australia.