NDLI: IL-21 promotes CD4 T cell responses by phosphatidylinositol 3-kinase-dependent upregulation of CD86 on B cells.

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IL-21 promotes CD4 T cell responses by phosphatidylinositol 3-kinase-dependent upregulation of CD86 on B cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Qureshi, Omar S. Manzotti, Claire Walker, Lucy S. K. Wardzinski, Lukasz Wang, Chun Jing Okkenhaug, Klaus Kenefeck, Rupert Attridge, Kesley
Description	Author Affiliation: Attridge K ( Medical Research Council Centre for Immune Regulation, University of Birmingham Medical School, Birmingham B15 2TT, United Kingdom)
Abstract	The cytokine IL-21 is a potent immune modulator with diverse mechanisms of action on multiple cell types. IL-21 is in clinical use to promote tumor rejection and is an emerging target for neutralization in the setting of autoimmunity. Despite its clinical potential, the biological actions of IL-21 are not yet fully understood and the full range of effects of this pleiotropic cytokine are still being uncovered. In this study, we identify a novel role for IL-21 as an inducer of the costimulatory ligand CD86 on B lymphocytes. CD86 provides critical signals through T cell-expressed CD28 that promote T cell activation in response to Ag engagement. Expression levels of CD86 are tightly regulated in vivo, being actively decreased by regulatory T cells and increased in response to pathogen-derived signals. In this study, we demonstrate that IL-21 can trigger potent and sustained CD86 upregulation through a STAT3 and PI3K-dependent mechanism. We show that elevated CD86 expression has functional consequences for the magnitude of CD4 T cell responses both in vitro and in vivo. These data pinpoint CD86 upregulation as an additional mechanism by which IL-21 can elicit immunomodulatory effects.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1302082
Journal	The Journal of Immunology
Issue Number	5
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd86 Immunology B-lymphocytes Interleukins Phosphatidylinositol 3-kinases T-lymphocytes, Regulatory Up-regulation Animals Biosynthesis Genetics Cytology Metabolism Mice Mice, Inbred Balb C Mice, Knockout Stat3 Transcription Factor Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Thymic medullary epithelium and thymocyte self-tolerance require cooperation between CD28-CD80/86 and CD40-CD40L costimulatory pathways.

IL-21 promotes CD4 T cell responses by phosphatidylinositol 3-kinase-dependent upregulation of CD86 on B cells.

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IL-21 promotes CD4 T cell responses by phosphatidylinositol 3-kinase-dependent upregulation of CD86 on B cells.