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The life (and death) of CD4+ CD28(null) T cells in inflammatory diseases.

Dumitriu, IE (2015) The life (and death) of CD4+ CD28(null) T cells in inflammatory diseases. Immunology, 146 (2). pp. 185-193. ISSN 1365-2567 https://doi.org/10.1111/imm.12506
SGUL Authors: Dumitriu, Ingrid Elena

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Abstract

Inflammation contributes to the development and perpetuation of several disorders and T lymphocytes orchestrate the inflammatory immune response. Although the role of T cells in inflammation is widely recognized, specific therapies that tackle inflammatory networks in disease are yet to be developed. CD4(+) CD28(null) T cells are a unique subset of helper T lymphocytes that recently shot back into the limelight as potential catalysts of inflammation in several inflammatory disorders such as autoimmunity, atherosclerosis and chronic viral infections. In contrast to conventional helper T cells, CD4(+) CD28(null) T cells have an inbuilt ability to release inflammatory cytokines and cytotoxic molecules that can damage tissues and amplify inflammatory pathways. It comes as no surprise that patients who have high numbers of these cells have more severe disease and poor prognosis. In this review, I provide an overview on the latest advances in the biology of CD4(+) CD28(null) T cells. Understanding the complex functions and dynamics of CD4(+) CD28(null) T cells may open new avenues for therapeutic intervention to prevent progression of inflammatory diseases.

Item Type: Article
Additional Information: This is the peer reviewed version of the following article: Dumitriu, I. E. (2015), The life (and death) of CD4+CD28null T cells in inflammatory diseases. Immunology, 146: 185–193., which has been published in final form at http://doi.org/10.1111/imm.12506. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
Keywords: CD4+CD28null T lymphocytes, apoptosis, atherosclerosis, autoimmunity, co-stimulation, helper T cells, inflammation, Animals, Anti-Inflammatory Agents, Antigens, CD28, Cell Death, Cell Proliferation, Cytokines, Cytotoxicity, Immunologic, Humans, Inflammation, Inflammation Mediators, Lymphocyte Activation, Phenotype, Prognosis, Severity of Illness Index, Signal Transduction, T-Lymphocytes, Helper-Inducer, T-Lymphocytes, Helper-Inducer, Animals, Humans, Inflammation, Antigens, CD28, Anti-Inflammatory Agents, Inflammation Mediators, Cytokines, Prognosis, Severity of Illness Index, Lymphocyte Activation, Signal Transduction, Cell Death, Cell Proliferation, Cytotoxicity, Immunologic, Phenotype, autoimmunity, apoptosis, atherosclerosis, co-stimulation, inflammation, CD4(+) CD28(null) T lymphocytes, helper T cells, Immunology, 1107 Immunology, 1114 Paediatrics And Reproductive Medicine
SGUL Research Institute / Research Centre: Academic Structure > Molecular and Clinical Sciences Research Institute (MCS)
Academic Structure > Molecular and Clinical Sciences Research Institute (MCS) > Cardiac (INCCCA)
Journal or Publication Title: Immunology
ISSN: 1365-2567
Language: eng
Dates:
DateEvent
October 2015Published
20 July 2015Published Online
10 July 2015Accepted
Publisher License: Publisher's own licence
Projects:
Project IDFunderFunder ID
PG/10/50/28434British Heart FoundationUNSPECIFIED
PG/13/24/30115British Heart FoundationUNSPECIFIED
PG/14/18/30724British Heart FoundationUNSPECIFIED
PubMed ID: 26190355
Web of Science ID: WOS:000362847500001
Go to PubMed abstract
URI: https://openaccess.sgul.ac.uk/id/eprint/107601
Publisher's version: https://doi.org/10.1111/imm.12506

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