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
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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: |
Date | Event |
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October 2015 | Published | 20 July 2015 | Published Online | 10 July 2015 | Accepted |
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Publisher License: |
Publisher's own licence |
Projects: |
Project ID | Funder | Funder ID |
---|
PG/10/50/28434 | British Heart Foundation | UNSPECIFIED | PG/13/24/30115 | British Heart Foundation | UNSPECIFIED | PG/14/18/30724 | British Heart Foundation | UNSPECIFIED |
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PubMed ID: |
26190355 |
Web of Science ID: |
WOS:000362847500001 |
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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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