| First Author | Xu X | Year | 2017 |
| Journal | J Immunol Res | Volume | 2017 |
| Pages | 3469108 | PubMed ID | 29250557 |
| Mgi Jnum | J:313208 | Mgi Id | MGI:6791631 |
| Doi | 10.1155/2017/3469108 | Citation | Xu X, et al. (2017) Stabilized beta-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice. J Immunol Res 2017:3469108 |
| abstractText | Autoimmune lymphoproliferative syndrome (ALPS) is an incurable disease mainly caused by the defect of Fas-mediated apoptosis and characterized by nonmalignant autoimmune lymphoproliferation. Stabilized beta-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 beta-cat(Tg) into lpr/lpr mice and aimed to explore the potential role of stabilized beta-catenin (beta-cat(Tg)) 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 beta-cat(Tg)lpr/lpr mice, especially the CD4 and CD8 TEM cells were significantly reduced. Meanwhile, stabilized beta-catenin obviously decreased the numbers of spleen TCRbeta(+)CD4(-)CD8(-) T (DNT) cells, and the levels of some serum proinflammatory factors also were lowered in beta-cat(Tg)lpr/lpr mice. Beyond that, stabilized beta-catenin slightly lowered the levels of the serum autoantibodies and the scores of kidney histopathology of beta-cat(Tg)lpr/lpr mice compared with lpr/lpr mice. Our study suggested that stabilized beta-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. |
