Support is requested for a Keystone Symposia conference entitled Cell Death and Inflammation, organized by Drs. Pascal Meier, Eric H. Baehrecke and Kim Newton. The conference will be held January 21 - 25, 2018 at Beaver Run Resort, Colorado. Cell death and inflammation are ancient processes of fundamental biological importance in both normal physiology and human disease pathologies. The recent observation that cell death regulatory components have dual roles in cell death and inflammation suggests that these proteins function not primarily to kill, but to coordinate tissue repair and adaptation to tissue stress. This perspective unifies cell death components as positive regulators of tissue repair that replaces malfunctioning or damaged tissues and enhances the resilience of epithelia to insult. It is now recognized that cells that die do not do so silently, but release a variety of paracrine signals to communicate with their cellular environment to ensure tissue regeneration and wound healing. Moreover, inflammatory signaling pathways, such as those emanating from the TNF-receptor or Toll- related receptors, take part in cell competition to eliminate developmentally aberrant clones. Understanding how dead and dying cells initiate and escalate inflammation has important implications for the development of novel treatment strategies for diseases associated with aging, such as chronic inflammation and cancer. This conference explores the complex relationship between cell death and inflammation, and how this cross-talk impacts on adaptation to tissue stress, inflammatory diseases, tumor formation and drug resistance. Overall, the goals of the conference are to: 1) Explore the gaps in our current understanding of how dead and dying cells influence inflammatory responses in tissue repair and disease settings; 2) Foster communication and collaborations between scientists focusing on different areas of biology (cell death, innate immunity, adaptive immunity, cancer and model organisms); 3) Pinpoint nodes of intersection linking all research fields;4) Define key-regulatory paradigms at these intersections, and discuss molecular mechanisms that control these processes; 5) Share information on possible consequences of deregulation; 6) Discuss translational aspects and potential drug targets, e.g. in pre-clinical models of malignant disease.
The recent observation that cell death regulatory components have dual roles in cell death and inflammation suggests that these proteins function not primarily to kill, but to coordinate tissue repair and adaptation to tissue stress. It is now recognized that cells that die do not do so silently, but release a variety of paracrine signals to communicate with their cellular environment to ensure tissue regeneration and wound healing. Understanding how dead and dying cells initiate and escalate inflammation has important implications for the development of novel treatment strategies for diseases associated with aging, such as chronic inflammation and cancer.
