NDLI: Differential T Cell Cytokine Receptivity and Not Signal Quality Distinguishes IL-6 and IL-10 Signaling during Th17 Differentiation.

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Differential T Cell Cytokine Receptivity and Not Signal Quality Distinguishes IL-6 and IL-10 Signaling during Th17 Differentiation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Bofeng Geiger, Terrence L. Alli, Rajshekhar Jones, Lindsay L.
Description	Author Affiliation: Jones LL ( Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105.); Alli R ( Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105.); Li B ( Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105.); Geiger TL ( Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105 terrence.geiger@stjude.org.)
Abstract	How a large number of cytokines differentially signal through a small number of signal transduction pathways is not well resolved. This is particularly true for IL-6 and IL-10, which act primarily through STAT3 yet induce dissimilar transcriptional programs leading alternatively to pro- and anti-inflammatory effects. Kinetic differences in signaling, sustained to IL-10 and transient to IL-6, are critical to this in macrophages. T cells are also key targets of IL-6 and IL-10, yet how differential signaling in these cells leads to divergent cellular fates is unclear. We show that, unlike for macrophages, signal duration cannot explain the distinct effects of these cytokines in T cells. Rather, naive, activated, activated-rested, and memory CD4(+) T cells differentially express IL-6 and IL-10 receptors in an activation state-dependent manner, and this impacts downstream cytokine effects. We show a dominant role for STAT3 in IL-6-mediated Th17 subset maturation. IL-10 cannot support Th17 differentiation because of insufficient cytokine receptivity rather than signal quality. Enforced expression of IL-10R on naive T cells permits an IL-10-generated STAT3 signal equivalent to that of IL-6 and equally capable of promoting Th17 formation. Similarly, naive T cell IL-10R expression also allows IL-10 to mimic the effects of IL-6 on both Th1/Th2 skewing and Tfh cell differentiation. Our results demonstrate a key role for the regulation of receptor expression rather than signal quality or duration in differentiating the functional outcomes of IL-6 and IL-10 signaling, and identify distinct signaling properties of these cytokines in T cells compared with myeloid cells.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	7
Volume Number	196
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2016-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Interleukin-10 Metabolism Interleukin-6 Signal Transduction Th17 Cells Cytology Animals Gene Expression Immunophenotyping Pharmacology Interleukin-10 Receptor Alpha Subunit Genetics Interleukin-6 Receptor Alpha Subunit Mice Mice, Transgenic Phenotype Stat3 Transcription Factor Drug Effects T-lymphocyte Subsets Immunology Th1 Cells Th2 Cells 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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Differential T Cell Cytokine Receptivity and Not Signal Quality Distinguishes IL-6 and IL-10 Signaling during Th17 Differentiation. : Correction

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Differential T Cell Cytokine Receptivity and Not Signal Quality Distinguishes IL-6 and IL-10 Signaling during Th17 Differentiation.

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Differential T Cell Cytokine Receptivity and Not Signal Quality Distinguishes IL-6 and IL-10 Signaling during Th17 Differentiation.