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Web Desc
Determinants of Host Resistance, Susceptibility or Immunopathology to Pathogens: Integrating Knowledge from Experimental Models to Human Disease
joint with Pathogen-Host Standoff: Persistent and Latent Infection
Organizer(s): Anne O'Garra, Anne E. Goldfeld, Alan Sher and Bruce D. Walker
Date: January 06 - 11, 2006
Location: Keystone Resort, Keystone, CO, USA
Supported by the Burroughs Wellcome Fund and The Director's Fund
Summary of Meeting:
The type of immune response that is elicited upon infection of a host with a pathogen is critical in determining whether the pathogen is eradicated or whether chronic infection ensues. Successful protective effector responses to intracellular pathogens such as parasites, bacteria and viruses are initiated by cells of the innate immune response which produce effector cytokines such as TNF, IL-12 or IFN-alpha. These, in turn, stimulate antigen-specific Th1 cells producing IFN-alpha and CD8+ T cytotoxic T cells (CTL). Humoral immune responses also offer protection against pathogens, however rapid mutations in the organisms and/or the lack of immunizing regimens which lead to long-term protection impede successful vaccination. Host mutations in cytokine signaling pathways and signaling pathways downstream of pattern recognition receptors on host immune cells result in profound susceptibility to a number of pathogens. Furthermore, many organisms -- such as Leishmania, Schistosoma or Mycobacteria -- inhibit protective immune responses via the induction of suppressive cytokines, whereas influenza has developed molecular mechanisms to interfere directly with signaling pathways important for the induction of the host antiviral response. Overall, major reasons why we have failed to-date in eliminating human pathogens are 1) successful strategies of immunoevasion developed by pathogens to dampen an immune response and, conversely, 2) pathogen-induced immunopathologies further complicate infections. Furthermore, the emergence and re-emergence of many infectious pathogens throughout human history, the difficulty in producing effective vaccines to protect against numerous pathogens, and the inability to intervene immunologically to abrogate many chronic infectious diseases such as HIV, malaria, TB, and schistosomiasis highlight the need for a deeper understanding of the immune response to infectious challenge. Cross-fertilization of knowledge gained from animal models of infectious disease with our understanding of human immune responses to a broad range of pathogens is critical to advance the treatment and prevention of devastating pathogens.
Scholarship Deadline: September 13 2005
Discounted Abstract Deadline: September 13 2005
Abstract Deadline: October 3 2005
Discounted Registration Deadline: November 4 2005
We gratefully acknowledge additional support for this conference from:
Burroughs Wellcome Fund
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Merck Vaccine Division
We gratefully acknowledge the generous grant for this conference provided by:

National Institute of Allergy and Infectious Diseases (NIAID)
Grant No. 1 R13 AI066871-01
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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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