%0 Journal Article
%T Stabilized β-Catenin Ameliorates ALPS-Like Symptoms of B6/lpr Mice.
%A Xu X
%A Huang J
%A Zhao M
%A Chen H
%A Mo J
%A Zhou X
%A Su Q
%A Yu B
%A Huang Z
%J J Immunol Res
%V 2017
%N 0
%D 2017
%M 29250557
%F 4.493
%R 10.1155/2017/3469108
%X 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.