Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice
Autoimmune lymphoproliferative syndrome (ALPS) is an incurable disease mainly caused by the defect of Fas-mediated apoptosis and characterized by nonmalignant autoimmune lymphoproliferation. Stabilized β-catenin could not only potentiate Fas-mediated T cell apoptosis via upregulating the expression...
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2017-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2017/3469108 |
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author | Xiaoxie Xu Jun Huang Mei Zhao Huanpeng Chen Jinhua Mo Xiaoqing Zhou Qiao Su Bolan Yu Zhaofeng Huang |
author_facet | Xiaoxie Xu Jun Huang Mei Zhao Huanpeng Chen Jinhua Mo Xiaoqing Zhou Qiao Su Bolan Yu Zhaofeng Huang |
author_sort | Xiaoxie Xu |
collection | DOAJ |
description | Autoimmune lymphoproliferative syndrome (ALPS) is an incurable disease mainly caused by the defect of Fas-mediated apoptosis and characterized by nonmalignant autoimmune lymphoproliferation. Stabilized β-catenin could not only potentiate Fas-mediated T cell apoptosis via upregulating the expression of Fas on activated T cells, but also potentiate T cell apoptosis via intrinsic apoptotic pathway. In the present study, we introduced β-catTg into lpr/lpr mice and aimed to explore the potential role of stabilized β-catenin (β-catTg) in the development of ALPS-like phenotypes of lpr/lpr mice. We found that the total splenocyte cells and some compositions were slightly downregulated in β-catTglpr/lpr mice, especially the CD4 and CD8 TEM cells were significantly reduced. Meanwhile, stabilized β-catenin obviously decreased the numbers of spleen TCRβ+CD4−CD8− T (DNT) cells, and the levels of some serum proinflammatory factors also were lowered in β-catTglpr/lpr mice. Beyond that, stabilized β-catenin slightly lowered the levels of the serum autoantibodies and the scores of kidney histopathology of β-catTglpr/lpr mice compared with lpr/lpr mice. Our study suggested that stabilized β-catenin ameliorated some ALPS-like symptoms of lpr/lpr mice by potentiating Fas-independent signal-mediated T cell apoptosis, which might uncover a potential novel therapeutic direction for ALPS. |
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institution | Kabale University |
issn | 2314-8861 2314-7156 |
language | English |
publishDate | 2017-01-01 |
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series | Journal of Immunology Research |
spelling | doaj-art-57529715faf54a6394fa181d8c54d1c92025-02-03T07:24:32ZengWileyJournal of Immunology Research2314-88612314-71562017-01-01201710.1155/2017/34691083469108Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr MiceXiaoxie Xu0Jun Huang1Mei Zhao2Huanpeng Chen3Jinhua Mo4Xiaoqing Zhou5Qiao Su6Bolan Yu7Zhaofeng Huang8Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, ChinaKey Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, ChinaInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, ChinaKey Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, ChinaAnimal Experiment Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, ChinaKey Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, ChinaAutoimmune lymphoproliferative syndrome (ALPS) is an incurable disease mainly caused by the defect of Fas-mediated apoptosis and characterized by nonmalignant autoimmune lymphoproliferation. Stabilized β-catenin could not only potentiate Fas-mediated T cell apoptosis via upregulating the expression of Fas on activated T cells, but also potentiate T cell apoptosis via intrinsic apoptotic pathway. In the present study, we introduced β-catTg into lpr/lpr mice and aimed to explore the potential role of stabilized β-catenin (β-catTg) in the development of ALPS-like phenotypes of lpr/lpr mice. We found that the total splenocyte cells and some compositions were slightly downregulated in β-catTglpr/lpr mice, especially the CD4 and CD8 TEM cells were significantly reduced. Meanwhile, stabilized β-catenin obviously decreased the numbers of spleen TCRβ+CD4−CD8− T (DNT) cells, and the levels of some serum proinflammatory factors also were lowered in β-catTglpr/lpr mice. Beyond that, stabilized β-catenin slightly lowered the levels of the serum autoantibodies and the scores of kidney histopathology of β-catTglpr/lpr mice compared with lpr/lpr mice. Our study suggested that stabilized β-catenin ameliorated some ALPS-like symptoms of lpr/lpr mice by potentiating Fas-independent signal-mediated T cell apoptosis, which might uncover a potential novel therapeutic direction for ALPS.http://dx.doi.org/10.1155/2017/3469108 |
spellingShingle | Xiaoxie Xu Jun Huang Mei Zhao Huanpeng Chen Jinhua Mo Xiaoqing Zhou Qiao Su Bolan Yu Zhaofeng Huang Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice Journal of Immunology Research |
title | Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice |
title_full | Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice |
title_fullStr | Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice |
title_full_unstemmed | Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice |
title_short | Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice |
title_sort | stabilized β catenin ameliorates alps like symptoms of b6 lpr mice |
url | http://dx.doi.org/10.1155/2017/3469108 |
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