joint with the meeting on Integrating Metabolism and Immunity
Cell death has long been known to be an important instigator of inflammation in sterile injury, as well as an amplifying factor in infection-associated inflammation, but the specific molecules underpinning this remain obscure. Understanding how dead and dying cells initiate and escalate inflammation has important implications for our understanding and treatment of autoinflammatory and infectious diseases. This meeting will explore current knowledge concerning the cellular constituents that drive inflammation (i.e., damage-associated molecular patterns), as well as how abnormal modes of cell death, such as necrosis, necroptosis and NETosis, can perturb inflammatory outputs and responses to dying cells. In particular, the conference aims to explore gaps in our current understanding of how dead and dying cells influence inflammatory responses in disease settings and will bring together experts in two major research fields, ”cell death” and ”inflammation,” for the purpose of clarifying what the key questions and therapeutic targets are in this rapidly evolving area. Many well-known physiological drivers of cell death (e.g., TNF, TRAIL, CD95/Fas), as well as the molecules that transduce signals from these receptors (e.g., RIPKs, IAPs, TRAFs, IKKs), are also centrally involved in promoting inflammation. However, the tremendous overlap between cell death and inflammatory signaling is only becoming appreciated of late, and although it is also widely accepted that the constituents of healthy cells can drive inflammation upon release into the extracellular space, the identity of these cellular constituents is still a matter of debate. This meeting will focus on teasing out the relationships between cell death and inflammatory signaling to highlight how perturbation of either of these processes invariably impacts upon the other. This meeting will also explore the nature of the molecules that promote and modulate inflammation during cell death. The meeting will bring together scientists from diverse fields (cell death, inflammation, cancer, innate immunity) that would not normally interact, and will identify and explore the key questions and directions that will shape the future of research in this field.
Abstract & Scholarship Deadline: January 31, 2017
Abstract Deadline: March 1, 2017
Discounted Registration Deadline: March 29, 2017
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