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Web Desc
Type I Interferon: Friend and Foe Alike
joint with Pattern Recognition Signaling: From Innate Immunity to Inflammatory Disease
Organizer(s): Alan Sher, Virginia Pascual, Adolfo García-Sastre and Anne O'Garra
Date: March 19 - 23, 2017
Location: Fairmont Banff Springs, Banff, AB, Canada
Supported by the Directors' Fund
Summary of Meeting:
While cytokines play critical roles in host defense and immune homeostasis, they in other settings can be key mediators of inflammatory pathology. This important functional dichotomy is perhaps best exemplified in the diverse activities of Type I interferon(s) in health and disease. Type I IFNs regulate a broad family of genes that either stimulate or inhibit immune function and in so doing have host protective or detrimental effects. Thus, while Type I IFNs are well-known for their anti-viral activity and stimulation of effector T cell responses, they can also promote autoimmune, bacterial and even certain viral diseases. Understanding this contextual dependency is crucial for unraveling the pathogenesis of Type I IFN-dependent diseases and for the design of interferon-based therapies and will be the central focus of the meeting. The conference will open with talks presenting an overview of Type I IFN genes and their regulation, innate recognition mechanisms and signaling pathways for Type I IFN induction and Mendelian-based interferonopathies. Additional sessions will focus on the role of Type I IFN in viral, bacterial and autoimmune diseases. The symposium will conclude with a discussion of the mechanistic and contextual factors that determine the beneficial versus deleterious outcome of Type I IFN induction and how this information can be applied to the development of targeted therapeutic interventions. Because of the timeliness of the topic, the conference should draw a broad audience from the fields of cytokine biology, inflammation, infectious disease and translational medicine and attract a solid industry representation.
Scholarship Deadline: November 17 2016
Discounted Abstract Deadline: November 17 2016
Abstract Deadline: December 20 2016
Discounted Registration Deadline: January 19 2017
We gratefully acknowledge additional support for this conference from:
CEDARLANE
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Genentech, Inc.

MedImmune
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:
Arthritis Research & Therapy (published by BioMed Central Ltd)
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Allergy and Infectious Diseases (NIAID)
Grant No. 1R13AI128981-01
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.
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

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Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

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