Adrian F. Ochsenbein

Bernhard Odermatt

Burkhard Ludewig

Cornelis J. M. Melief

Hans Hengartner

Kathy McCoy

Marcus Pericin

Rene E. M. Toes

Rolf M. Zinkernagel

Tilman Dumrese

Abstract
               This study evaluated to what extent presentation of exogenously acquired self-Ags via MHC class I molecules on DC might contribute to the activation of self-reactive CTL and subsequent development of autoimmune disease. We show here by using the rat insulin promotor lymphocytic choriomeningitis virus glycoprotein model of autoimmune diabetes that the activation of self-reactive CTL by DC after uptake of exogenous Ag is very limited, first by the short half-life of MHC class I-associated peptides on DC in vitro and in vivo, and second by the rather inefficient MHC class I presentation of cell-associated self-Ags by DC. These two mechanisms are probably crucial in establishing high thresholds for the induction of self-reactive CTL that prevent autoimmune sequelae after release of sequestered and previously immunologically ignored tissue Ags.</jats:p

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The Journal of Immunology

Rapid Peptide Turnover and Inefficient Presentation of Exogenous Antigen Critically Limit the Activation of Self-Reactive CTL by Dendritic Cells

Rapid Peptide Turnover and Inefficient Presentation of Exogenous Antigen Critically Limit the Activation of Self-Reactive CTL by Dendritic Cells

Abstract

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