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TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice

Dendritic cells (DCs) are important in the initiation of primary T‐cell responses, while transforming growth factor‐β (TGF‐β)‐activated kinase 1 (TAK1) is a critical regulator of DC survival and homeostasis. This study evaluated the T‐cell dependent antibody response (TDAR) to sheep red blood cells...

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Detalles Bibliográficos
Autores principales: Pan, Yao, Lei, Zhiming, Wei, Xuetao, Hao, Weidong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887970/
https://www.ncbi.nlm.nih.gov/pubmed/27419057
http://dx.doi.org/10.1002/2211-5463.12062
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author Pan, Yao
Lei, Zhiming
Wei, Xuetao
Hao, Weidong
author_facet Pan, Yao
Lei, Zhiming
Wei, Xuetao
Hao, Weidong
author_sort Pan, Yao
collection PubMed
description Dendritic cells (DCs) are important in the initiation of primary T‐cell responses, while transforming growth factor‐β (TGF‐β)‐activated kinase 1 (TAK1) is a critical regulator of DC survival and homeostasis. This study evaluated the T‐cell dependent antibody response (TDAR) to sheep red blood cells (SRBC) on a DC‐specific TAK1‐deficient mice model. The results showed that TAK1 deficiency in DCs significantly suppressed the humoral and cellular immune response in mice. DC‐specific TAK1 deletion impaired splenic T‐cell population and conventional DCs, abolished the cytokine production of splenic T cells and down‐regulated some functional gene expression in the spleen. Collectively, this study suggests that TAK1 plays an essential role in the development of the humoral immune response.
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spelling pubmed-48879702016-07-14 TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice Pan, Yao Lei, Zhiming Wei, Xuetao Hao, Weidong FEBS Open Bio Research Articles Dendritic cells (DCs) are important in the initiation of primary T‐cell responses, while transforming growth factor‐β (TGF‐β)‐activated kinase 1 (TAK1) is a critical regulator of DC survival and homeostasis. This study evaluated the T‐cell dependent antibody response (TDAR) to sheep red blood cells (SRBC) on a DC‐specific TAK1‐deficient mice model. The results showed that TAK1 deficiency in DCs significantly suppressed the humoral and cellular immune response in mice. DC‐specific TAK1 deletion impaired splenic T‐cell population and conventional DCs, abolished the cytokine production of splenic T cells and down‐regulated some functional gene expression in the spleen. Collectively, this study suggests that TAK1 plays an essential role in the development of the humoral immune response. John Wiley and Sons Inc. 2016-04-21 /pmc/articles/PMC4887970/ /pubmed/27419057 http://dx.doi.org/10.1002/2211-5463.12062 Text en © 2016 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Pan, Yao
Lei, Zhiming
Wei, Xuetao
Hao, Weidong
TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title_full TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title_fullStr TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title_full_unstemmed TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title_short TAK1 deficiency in dendritic cells inhibits adaptive immunity in SRBC‐immunized C57BL/6 mice
title_sort tak1 deficiency in dendritic cells inhibits adaptive immunity in srbc‐immunized c57bl/6 mice
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887970/
https://www.ncbi.nlm.nih.gov/pubmed/27419057
http://dx.doi.org/10.1002/2211-5463.12062
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