CD161 is a marker of all human IL‐17‐producing T‐cell subsets and is induced by RORC

L Maggi, V Santarlasci, M Capone… - European journal of …, 2010 - Wiley Online Library
L Maggi, V Santarlasci, M Capone, A Peired, F Frosali, SQ Crome, V Querci, M Fambrini…
European journal of immunology, 2010Wiley Online Library
We have previously shown that human Th17 lymphocytes are characterized by the selective
expression of IL‐23 receptor (IL‐23R), CCR6, CD161, and the transcription factor retinoic
acid‐related orphan receptor C (RORC), and originate from a CD161+ CD4+ naïve T‐cell
precursor in response to the combined activity of IL‐1β and IL‐23. We show here that not
only CD4+ TCRαβ+, but also CD8+ TCRαβ+, CD4− CD8− TCRαβ+, and CD4− CD8−
TCRγδ+ circulating lymphocytes that produce IL‐17 express the distinctive marker CD161 …
Abstract
We have previously shown that human Th17 lymphocytes are characterized by the selective expression of IL‐23 receptor (IL‐23R), CCR6, CD161, and the transcription factor retinoic acid‐related orphan receptor C (RORC), and originate from a CD161+CD4+ naïve T‐cell precursor in response to the combined activity of IL‐1β and IL‐23. We show here that not only CD4+TCRαβ+, but also CD8+TCRαβ+, CD4CD8 TCRαβ+, and CD4CD8 TCRγδ+ circulating lymphocytes that produce IL‐17 express the distinctive marker CD161 on their surface. In addition, we demonstrate that CD161 expression identifies CD8+ and CD4CD8 umbilical cord blood T cells that already express RORC and IL‐23R mRNA and that can be induced to differentiate into IL‐17‐producing cells in the presence of IL‐1β and IL‐23. Finally, we provide evidence that umbilical cord blood naïve CD4+CD161 T cells, upon lentivirus‐mediated transduction with RORC2 can acquire the ability to express IL‐23R, IL‐1RI, and CD161, as well as to produce IL‐17. Taken together, these data allow to conclude that T‐cell subsets able to produce IL‐17, as well as precursors of IL‐17‐producing T cells, exhibit surface expression of CD161, and that this feature is at least in part RORC2‐dependent.
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