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The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency
In this study, we showed the direct interaction between Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein (FAP) and toll-like receptor4 (TLR4) via co-localization and binding by using confocal microscopy and co-immunoprecipitation assays. FAP triggered the expression of pro-...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Korean Society for Biochemistry and Molecular Biology
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366327/ https://www.ncbi.nlm.nih.gov/pubmed/22322306 http://dx.doi.org/10.3858/emm.2012.44.5.038 |
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author | Noh, Kyung Tae Shin, Sung Jae Son, Kwang Hee Jung, In Duk Kang, Hyun Kyu Lee, Su Jung Lee, Eun Kyung Shin, Yong Kyoo You, Ji Chang Park, Yeong-Min |
author_facet | Noh, Kyung Tae Shin, Sung Jae Son, Kwang Hee Jung, In Duk Kang, Hyun Kyu Lee, Su Jung Lee, Eun Kyung Shin, Yong Kyoo You, Ji Chang Park, Yeong-Min |
author_sort | Noh, Kyung Tae |
collection | PubMed |
description | In this study, we showed the direct interaction between Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein (FAP) and toll-like receptor4 (TLR4) via co-localization and binding by using confocal microscopy and co-immunoprecipitation assays. FAP triggered the expression of pro- and anti-inflammatory cytokines in a TLR4-dependent manner. In addition, FAP-induced cytokine expression in bone marrow-derived dendritic cells (BMDCs) was modulated in part by glycogen synthase kinase-3 (GSK-3). FAP-induced expression of CD80, CD86, major histocompatibility complex (MHC) class I, and MHC class II in TLR4(+/+) BMDCs was not observed in TLR4(-/-) BMDCs. Furthermore, FAP induced DC-mediated CD8(+) T cell proliferation and cytotoxic T lymphocyte (CTL) activity, and suppressed tumor growth with DC-based tumor vaccination in EG7 thymoma murine model. Taken together, these results indicate that the TLR4 agonist, FAP, a potential immunoadjuvant for DC-based cancer vaccination, improves the DC-based immune response via the TLR4 signaling pathway. |
format | Online Article Text |
id | pubmed-3366327 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Korean Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-33663272012-06-07 The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency Noh, Kyung Tae Shin, Sung Jae Son, Kwang Hee Jung, In Duk Kang, Hyun Kyu Lee, Su Jung Lee, Eun Kyung Shin, Yong Kyoo You, Ji Chang Park, Yeong-Min Exp Mol Med Original Article In this study, we showed the direct interaction between Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein (FAP) and toll-like receptor4 (TLR4) via co-localization and binding by using confocal microscopy and co-immunoprecipitation assays. FAP triggered the expression of pro- and anti-inflammatory cytokines in a TLR4-dependent manner. In addition, FAP-induced cytokine expression in bone marrow-derived dendritic cells (BMDCs) was modulated in part by glycogen synthase kinase-3 (GSK-3). FAP-induced expression of CD80, CD86, major histocompatibility complex (MHC) class I, and MHC class II in TLR4(+/+) BMDCs was not observed in TLR4(-/-) BMDCs. Furthermore, FAP induced DC-mediated CD8(+) T cell proliferation and cytotoxic T lymphocyte (CTL) activity, and suppressed tumor growth with DC-based tumor vaccination in EG7 thymoma murine model. Taken together, these results indicate that the TLR4 agonist, FAP, a potential immunoadjuvant for DC-based cancer vaccination, improves the DC-based immune response via the TLR4 signaling pathway. Korean Society for Biochemistry and Molecular Biology 2012-05-31 2012-02-09 /pmc/articles/PMC3366327/ /pubmed/22322306 http://dx.doi.org/10.3858/emm.2012.44.5.038 Text en Copyright © 2012 by the Korean Society for Biochemistry and Molecular Biology http://creativecommons.org/licenses/by-nc/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Noh, Kyung Tae Shin, Sung Jae Son, Kwang Hee Jung, In Duk Kang, Hyun Kyu Lee, Su Jung Lee, Eun Kyung Shin, Yong Kyoo You, Ji Chang Park, Yeong-Min The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title | The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title_full | The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title_fullStr | The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title_full_unstemmed | The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title_short | The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
title_sort | mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366327/ https://www.ncbi.nlm.nih.gov/pubmed/22322306 http://dx.doi.org/10.3858/emm.2012.44.5.038 |
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