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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kaplan, Mark H. Stritesky, Gretta L. Yeh, Norman
Description	Country affiliation: United States Author Affiliation: Stritesky GL ( Department of Pediatrics, HB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.)
Abstract	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-1beta. 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.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	9
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Immunology Cell Lineage Interleukin-17 Biosynthesis Interleukin-23 Physiology T-lymphocytes, Helper-inducer Metabolism Animals Cell Division Cell Proliferation Cell Survival Cells, Cultured Immunophenotyping Secretion Lymphocyte Activation Mice Mice, Inbred Balb C Mice, Inbred C57bl Cytology Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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