Cell death is an essential biological process in life, required to remove old or harmful cells. It plays
a crucial role during development, regeneration and homeostasis. Cell death and survival have to
be tightly regulated in order to maintain a good balance necessary for the function of an organism.
Loss of this balanced regulation will result in deviation from homeostatic conditions, manifesting
in various diseases. In this project we will focus on a protein that has a multifaceted function in cell
death and survival. This protein receptor interacting protein kinase 1 (RIPK1) paradoxically
functions as cell death mediator and as survival mediator depending on cell types and cellular
context. Deletion of RIPK1 in whole body is lethal in mice. Therefore, we engineered mice that lack
RIPK1 in selected tissues. In this project we will study the mice lacking RIPK1 in T lymphocytes,
cells of the adaptive immune system that play a central role in immunity. Surprisingly, those mice
developed inflammation in various tissues that are covering body cavity or surface of organs such
as intestine, lung and skin. This intriguing observation suggests that altered survival or altered
function of T cells exerts a profound impact on inflammation in multiple locations. We will
investigate into this vastly unknown territory by examining the function of RIPK1 in T cells.