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Article
Nature Medicine  9, 1469 - 1476 (2003)
Published online: 16 November 2003; | doi:10.1038/nm962

Hsp70 promotes antigen-presenting cell function and converts T-cell tolerance to autoimmunity in vivo

Douglas G Millar1, Kristine M Garza2, Bernhard Odermatt3, Alisha R Elford1, Nobuyuki Ono1, Zihai Li4 & Pamela S Ohashi1

1  Departments of Immunology and Medical Biophysics, University Health Network, Ontario Cancer Institute, Toronto, Ontario M5G 2M9, Canada.

2  Department of Biological Sciences, University of Texas at El Paso, El Paso, Texas 79968, USA.

3  Institute of Pathology, Department of Experimental Pathology, University Hospital, 8091 Zurich, Switzerland.

4  Center for Immunotherapy of Cancer and Infectious Diseases, University of Connecticut, Farmington, Connecticut 06030, USA.

Correspondence should be addressed to Pamela S Ohashi pohashi@uhnres.utoronto.ca
Pathogens or pathogen-associated molecular patterns can signal to cells of the innate immune system and trigger effective adaptive immunity. However, relatively little is known about how the innate immune system detects tissue injury or necrosis. Evidence suggests that the release of heat-shock proteins (HSPs) may provide adjuvant-like signals, but the ability of HSPs to promote activation or tolerance in vivo has not been addressed. In this study we show that Hsp70 promotes dendritic cell (DC) function and, together with antigen, triggers autoimmune disease in vivo.

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Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
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