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Web Desc
Cell Death, Inflammation and Adaptation to Tissue Stress
Organizer(s): Pascal Meier, Eric H. Baehrecke and Kim Newton
Date: January 21 - 25, 2018
Location: Beaver Run Resort, Breckenridge, CO, USA
Sponsored by Akebia Therapeutics, Amgen Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Cancer Research UK, Genentech, Inc. and Roche
Summary of Meeting:
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 replace 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.
Scholarship Deadline: September 27 2017
Discounted Abstract Deadline: September 27 2017
Abstract Deadline: October 25 2017
Discounted Registration Deadline: November 28 2017
Keystone Symposia thanks our Sponsor(s) for generously supporting this meeting:
Akebia Therapeutics
Amgen Inc.
Boehringer Ingelheim Pharmaceuticals, Inc.Cancer Research UKGenentech, Inc.Roche
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Genentech, Inc.
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Allergy and Infectious Diseases (NIAID)
Grant No. 1 R13 AI136036-01
Funding for this conference was made possible (in part) by 1 R13 AI136036-01 from the National Institutes of Health. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.
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