David R Fernandez, Tiffany Telarico, Eduardo Bonilla, Qing Li, Sanjay Banerjee, Frank A Middleton, Paul E Phillips, Mary K Crow, Stefanie Oess, Werner Muller-Esterl, Andras Perl
Persistent mitochondrial hyperpolarization (MHP) and enhanced calcium fluxing underlie aberrant T cell activation and death pathway selection in systemic lupus erythematosus. Treatment with rapamycin, which effectively controls disease activity, normalizes CD3/CD28-induced calcium fluxing but fails to influence MHP, suggesting that altered calcium fluxing is downstream or independent of mitochondrial dysfunction. In this article, we show that activity of the mammalian target of rapamycin (mTOR), which is a sensor of the mitochondrial transmembrane potential, is increased in lupus T cells...
February 15, 2009: Journal of Immunology