IL-23 promotes maintenance but not commitment to the Th17 lineage

Gretta L. Stritesky, Norman Yeh, Mark H. Kaplan

Research output: Contribution to journalArticlepeer-review

232 Scopus citations


IL-23 plays a critical role establishing inflammatory immunity and enhancing IL-17 production in vivo. However, an understanding of how it performs those functions has been elusive. In this report, using an IL-17-capture technique, we demonstrate that IL-23 maintains the IL-17-secreting phenotype of purified IL-17+ cells without affecting cell expansion or survival. IL-23 maintains the Th17 phenotype over multiple rounds of in vitro stimulation most efficiently in conjunction with IL-1β. However, in contrast to Th1 and Th2 cells, the Th17 phenotype is not stable and when long-term IL-23-stimulated Th17 cultures are exposed to Th1- or Th2-inducing cytokines, the Th17 genetic program is repressed and cells that previously secreted IL-17 assume the cytokine secreting profile of other Th subsets. Thus, while IL-23 can maintain the Th17 phenotype, it does not promote commitment to an IL-17-secreting lineage.

Original languageEnglish (US)
Pages (from-to)5948-5955
Number of pages8
JournalJournal of Immunology
Issue number9
StatePublished - Nov 1 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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