NDLI: Prostaglandin E2 affects T cell responses through modulation of CD46 expression.

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Prostaglandin E2 affects T cell responses through modulation of CD46 expression.

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Prostaglandin E2 affects T cell responses through modulation of CD46 expression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Maltby, Kathryn Wright, Sheila Ni Choileain, Siobhán Jabbour, Henry N. Astier, Anne L. Stephen, Jillian Kickler, Karoline Hafler, David A.
Description	Country affiliation: United kingdom Author Affiliation: Kickler K ( Centre for Inflammation Research, University of Edinburgh, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom.)
Abstract	The ubiquitous protein CD46, a regulator of complement activity, promotes T cell activation and differentiation toward a regulatory Tr1-like phenotype. The CD46-mediated differentiation pathway is defective in several chronic inflammatory diseases, underlying the importance of CD46 in controlling T cell function and the need to understand its regulatory mechanisms. Using an RNA interference-based screening approach in primary T cells, we have identified that two members of the G protein-coupled receptor kinases were involved in regulating CD46 expression at the surface of activated cells. We have investigated the role of PGE(2), which binds to the E-prostanoid family of G protein-coupled receptors through four subtypes of receptors called EP 1-4, in the regulation of CD46 expression and function. Conflicting roles of PGE(2) in T cell functions have been reported, and the reasons for these apparent discrepancies are not well understood. We show that addition of PGE(2) strongly downregulates CD46 expression in activated T cells. Moreover, PGE(2) differentially affects T cell activation, cytokine production, and phenotype depending on the activation signals received by the T cells. This was correlated with a distinct pattern of the PGE(2) receptors expressed, with EP4 being preferentially induced by CD46 activation. Indeed, addition of an EP4 antagonist could reverse the effects observed on cytokine production after CD46 costimulation. These data demonstrate a novel role of the PGE(2)-EP4 axis in CD46 functions, which might at least partly explain the diverse roles of PGE(2) in T cell functions.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103090
Journal	The Journal of Immunology
Issue Number	11
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd46 Metabolism Dinoprostone Physiology Lymphocyte Activation Immunology T-lymphocyte Subsets Antagonists & Inhibitors Biosynthesis Cell Proliferation Cells, Cultured G-protein-coupled Receptor Kinase 1 Gene Expression Regulation Rna Interference Receptors, Prostaglandin E, Ep2 Subtype Receptors, Prostaglandin E, Ep4 Subtype Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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