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Distinctive expression of interleukin‐23 receptor subunits on human Th17 and γδ T cells
Author(s) -
Wines Bruce D,
Yap May L,
Powell Maree S,
Tan PeckSzee,
Ko K Kerry,
Orlowski Eva,
Hogarth P Mark
Publication year - 2017
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2016.93
Subject(s) - interleukin 12 receptor, beta 1 subunit , protein subunit , interleukin 23 , microbiology and biotechnology , interleukin 10 receptor, alpha subunit , biology , interleukin 17 , interleukin 3 , receptor , t cell , chemistry , interleukin 21 , g alpha subunit , immunology , inflammation , immune system , gene , biochemistry
The interleukin‐23 (IL‐23) pathway, T helper 17 (Th17) cells and γδ T cells, which respond to IL‐23, have major pro‐inflammatory roles. We have used unique IL‐23 receptor (IL‐23R) subunit‐specific monoclonal antibodies, X67 and X68, and IL‐12 receptor beta‐1 subunit (IL‐12Rβ1) expression levels to evaluate the IL‐23R complex on CD4 αβ TCR Th17 cells and on γδ T cells. Both IL‐23R and IL‐12Rβ1 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‐12Rβ1 subunit, which appeared a better predictor of responsiveness to IL‐23 than the expression of the IL‐23R subunit. Moreover, sorting memory CD4 T cells by high IL‐12Rβ1 expression selectively enriched cells committed to IL‐17 production from the blood. IL‐23R expression was also observed on freshly isolated and cultured γδ T cells and the cultured γδ T cells were not responsive to IL‐23.