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Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases
Autoimmune diseases are usually accompanied by tissue injury caused by autoantigen-specific T-cells. K(V)1.3 channels participate in modulating calcium signaling to induce T-cell proliferation, immune activation and cytokine production. Effector memory T (T(EM))-cells, which play major roles in many...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448172/ https://www.ncbi.nlm.nih.gov/pubmed/25996605 http://dx.doi.org/10.3390/toxins7051749 |
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author | Zhao, Yipeng Huang, Jie Yuan, Xiaolu Peng, Biwen Liu, Wanhong Han, Song He, Xiaohua |
author_facet | Zhao, Yipeng Huang, Jie Yuan, Xiaolu Peng, Biwen Liu, Wanhong Han, Song He, Xiaohua |
author_sort | Zhao, Yipeng |
collection | PubMed |
description | Autoimmune diseases are usually accompanied by tissue injury caused by autoantigen-specific T-cells. K(V)1.3 channels participate in modulating calcium signaling to induce T-cell proliferation, immune activation and cytokine production. Effector memory T (T(EM))-cells, which play major roles in many autoimmune diseases, are controlled by blocking K(V)1.3 channels on the membrane. Toxins derived from animal venoms have been found to selectively target a variety of ion channels, including K(V)1.3. By blocking the K(V)1.3 channel, these toxins are able to suppress the activation and proliferation of T(EM) cells and may improve T(EM) cell-mediated autoimmune diseases, such as multiple sclerosis and type I diabetes mellitus. |
format | Online Article Text |
id | pubmed-4448172 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-44481722015-06-01 Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases Zhao, Yipeng Huang, Jie Yuan, Xiaolu Peng, Biwen Liu, Wanhong Han, Song He, Xiaohua Toxins (Basel) Article Autoimmune diseases are usually accompanied by tissue injury caused by autoantigen-specific T-cells. K(V)1.3 channels participate in modulating calcium signaling to induce T-cell proliferation, immune activation and cytokine production. Effector memory T (T(EM))-cells, which play major roles in many autoimmune diseases, are controlled by blocking K(V)1.3 channels on the membrane. Toxins derived from animal venoms have been found to selectively target a variety of ion channels, including K(V)1.3. By blocking the K(V)1.3 channel, these toxins are able to suppress the activation and proliferation of T(EM) cells and may improve T(EM) cell-mediated autoimmune diseases, such as multiple sclerosis and type I diabetes mellitus. MDPI 2015-05-19 /pmc/articles/PMC4448172/ /pubmed/25996605 http://dx.doi.org/10.3390/toxins7051749 Text en © 2015 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 | Article Zhao, Yipeng Huang, Jie Yuan, Xiaolu Peng, Biwen Liu, Wanhong Han, Song He, Xiaohua Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title | Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title_full | Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title_fullStr | Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title_full_unstemmed | Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title_short | Toxins Targeting the K(V)1.3 Channel: Potential Immunomodulators for Autoimmune Diseases |
title_sort | toxins targeting the k(v)1.3 channel: potential immunomodulators for autoimmune diseases |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448172/ https://www.ncbi.nlm.nih.gov/pubmed/25996605 http://dx.doi.org/10.3390/toxins7051749 |
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