Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 9, Pages 5948-5955Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.9.5948
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Funding
- National Institutes of Health [AI45515]
- Training Grant in Immunology and Infectious Disease [T32AI060519]
- Indiana University Cancer Biology Training Program
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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 IIL-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-1 beta. 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. The Journal of Immunology, 2008, 181: 5948-5955.
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