Asymmetric cell division (ACD) is a conserved mechanism to establish differentiation, resulting in two daughter cells with differential potential fates. We compared the extent of ACD upon activation of different subsets of CD8+ T cells. Our results suggest that “stem” cells endowed with the ability to undergo clonal (re)expansion show higher ACD rates in comparison to cells that are unable to form a memory reservoir. Furthermore, we found that mTOR inhibition is able to increase ACD rates and that this reflects in daughter cells that, when transferred to new hosts and submitted to viral rechallenge, show better re-expansion and virus protection capacity.
I graduated in Biology in 2010 at the Federal University of Santa Catarina (UFSC) in Brazil. I was awarded a CNPq ‘scientific initiation’ fellowship from 2008 to 2010 and in that period I studied the immune system of Crustacea and developed monoclonal antibodies for immunodetection of shrimp viruses (Borsa et al., 2011; Seibert et al., 2010). I completed my Masters degree in Biotechnology and Biosciences also at UFSC in 2012. I was awarded a CAPES fellowship for the period of my Master studies about Unfolded Protein Response (UPR) activation by HIV infection (Borsa et al., 2015). I then worked as a Biology high school teacher in Brazil until I joined the lab of Annette Oxenius at ETHZ in 2014. During my PhD I have been working with asymmetric cell division in CD8 T lymphocytes and trying to understand how this mechanism impacts T cell fate and can be modulated to provide better memory potential and protection against viral infections.