Here, we report that NK cells from healthy human donors display increased killing of autologous B lymphoblastoid cell lines (LCLs) harboring latent EBV compared to primary B cells.
Similar to humans, these animals display increased pancreatic inflammation and associated beta cell death [9], [25].
In addition, it has been reported that obese humans and rodents display increased adipocyte apoptosis; further, apoptosis has been implicated in many neurodegenerative diseases including PD (Bharathi et al. 2006; Hirata 2002; Koh 2001; Ong and Farooqui 2005).
Moreover, we show that human CCM lesions display increased levels of p62/SQSTM1, an autophagic marker that accumulates when autophagy is inhibited.
Through retroviral expression of Wnt1, Ayyannan and coworkers were able to demonstrate that a subset of primary human mammary epithelial cells (HMECs) display increased proliferation, an ability to form multicellular spheres and a failure to senesce following exposure to Wnt1 for a period of several weeks [ 1].
Human Friedreich ataxia-derived lymphoblasts also display increased autophagy, indicating an evolutionarily conserved response to reduced frataxin expression.
They also display increased expression levels in various human tumors [10], [23].
β-cells from Hq mutant mice display increased sensitivity to hydrogen peroxide-induced apoptosis, which was confirmed in human islets in which AIF was depleted by siRNA.
Human nevi (moles) display many features of oncogene-induced senescence; they remain growth arrested for decades, display increased p16INK4a expression, stain positive for senescence-associated-ß-galactosidase (SA-ß-Gal) [ 1] and carry oncogenic mutations in the BRAF kinase [ 2].
Transgenic mice expressing human aSyn show pathogenic impairments of the mitochondrial function [ 14, 15] and conversely, aSyn-null mice often display increased resistance to MPTP [ 16, 17].
