Cargando…
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...
Autores principales: | , , , |
---|---|
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 |
_version_ | 1782354437518393344 |
---|---|
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. |
format | Online Article Text |
id | pubmed-4307281 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT venkateshashivaprasadh cytokinemodulatingstrategiesandnewercytokinetargetsforarthritistherapy AT dudicssteven cytokinemodulatingstrategiesandnewercytokinetargetsforarthritistherapy AT acharyabodhraj cytokinemodulatingstrategiesandnewercytokinetargetsforarthritistherapy AT moudgilkamald cytokinemodulatingstrategiesandnewercytokinetargetsforarthritistherapy |