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Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy

Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-17 can promote autoimmune pat...

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Autores principales: Venkatesha, Shivaprasad H., Dudics, Steven, Acharya, Bodhraj, Moudgil, Kamal D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307281/
https://www.ncbi.nlm.nih.gov/pubmed/25561237
http://dx.doi.org/10.3390/ijms16010887
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author Venkatesha, Shivaprasad H.
Dudics, Steven
Acharya, Bodhraj
Moudgil, Kamal D.
author_facet Venkatesha, Shivaprasad H.
Dudics, Steven
Acharya, Bodhraj
Moudgil, Kamal D.
author_sort Venkatesha, Shivaprasad H.
collection PubMed
description Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-17 can promote autoimmune pathology, whereas anti-inflammatory cytokines including IL-4, IL-10, and IL-27 can help control inflammation and tissue damage. The pro-inflammatory cytokines are the prime targets of the strategies to control rheumatoid arthritis (RA). For example, the neutralization of TNFα, either by engineered anti-cytokine antibodies or by soluble cytokine receptors as decoys, has proven successful in the treatment of RA. The activity of pro-inflammatory cytokines can also be downregulated either by using specific siRNA to inhibit the expression of a particular cytokine or by using small molecule inhibitors of cytokine signaling. Furthermore, the use of anti-inflammatory cytokines or cytokine antagonists delivered via gene therapy has proven to be an effective approach to regulate autoimmunity. Unexpectedly, under certain conditions, TNFα, IFN-γ, and few other cytokines can display anti-inflammatory activities. Increasing awareness of this phenomenon might help develop appropriate regimens to harness or avoid this effect. Furthermore, the relatively newer cytokines such as IL-32, IL-34 and IL-35 are being investigated for their potential role in the pathogenesis and treatment of arthritis.
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spelling pubmed-43072812015-02-02 Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy Venkatesha, Shivaprasad H. Dudics, Steven Acharya, Bodhraj Moudgil, Kamal D. Int J Mol Sci Review Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-17 can promote autoimmune pathology, whereas anti-inflammatory cytokines including IL-4, IL-10, and IL-27 can help control inflammation and tissue damage. The pro-inflammatory cytokines are the prime targets of the strategies to control rheumatoid arthritis (RA). For example, the neutralization of TNFα, either by engineered anti-cytokine antibodies or by soluble cytokine receptors as decoys, has proven successful in the treatment of RA. The activity of pro-inflammatory cytokines can also be downregulated either by using specific siRNA to inhibit the expression of a particular cytokine or by using small molecule inhibitors of cytokine signaling. Furthermore, the use of anti-inflammatory cytokines or cytokine antagonists delivered via gene therapy has proven to be an effective approach to regulate autoimmunity. Unexpectedly, under certain conditions, TNFα, IFN-γ, and few other cytokines can display anti-inflammatory activities. Increasing awareness of this phenomenon might help develop appropriate regimens to harness or avoid this effect. Furthermore, the relatively newer cytokines such as IL-32, IL-34 and IL-35 are being investigated for their potential role in the pathogenesis and treatment of arthritis. MDPI 2014-12-31 /pmc/articles/PMC4307281/ /pubmed/25561237 http://dx.doi.org/10.3390/ijms16010887 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Venkatesha, Shivaprasad H.
Dudics, Steven
Acharya, Bodhraj
Moudgil, Kamal D.
Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title_full Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title_fullStr Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title_full_unstemmed Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title_short Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy
title_sort cytokine-modulating strategies and newer cytokine targets for arthritis therapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307281/
https://www.ncbi.nlm.nih.gov/pubmed/25561237
http://dx.doi.org/10.3390/ijms16010887
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