HEAT-SHOCK INCREASES ANTIGENIC PEPTIDE GENERATION BUT DECREASES ANTIGEN PRESENTATION

The heat shock response is a universal and highly conserved cellular r esponse to stress. We describe here the effect of elevated temperature on the capacity of B cells to present antigen. Heat shock markedly af fects the ability of these cells to process and present tetanus toxin to class II-restricted T cell clones. Inhibition of antigen presentati on is due neither to a modification of antigen capture nor to a variat ion of major histocompatibility complex (MHC) class II molecule synthe sis and cell surface expression. Stressed and nonstressed B cells are able to present peptides loaded at the cell surface with the same effi ciency. Nevertheless, heat shock leads to an increase of antigen pepti de generation in subcellular compartments; an enhancement of cathepsin B activity is also observed. These data suggest that such a stress in duces a failure in the intracellular peptide loading onto MHC class II molecules.