Heat shock increases antigenic peptide generation but decreases antigen presentation.
The heat shock response is a universal and highly conserved cellular response to stress. We describe here the effect of elevated temperature on the capacity of B cells to present antigen. Heat shock markedly affects the ability of these cells to process and present tetanus toxin to class II-restricted T cell clones. Inhibition of antigen presentation is due neither to a modification of antigen capture nor to a variation of major histocompatibility complex (MHC) class II molecule synthesis and cell surface expression. Stressed and nonstressed B cells are able to present peptides loaded at the cell surface with the same efficiency. Nevertheless, heat shock leads to an increase of antigen peptide generation in subcellular compartments; an enhancement of cathepsin B activity is also observed. These data suggest that such a stress induces a failure in the intracellular peptide loading onto MHC class II molecules.
Pépin
E
E
Laboratoire d'Immunochimie, CEA-G, INSERM U238 and Université Joseph Fourier, Grenoble, France. PEPIN@dsvgre.cea.fr
Villiers
C L
CL
Gabert
F M
FM
Serra
V A
VA
Marche
P N
PN
Colomb
M G
MG
D000595:Amino Acid Sequence; D017951:Antigen Presentation / Q000528:radiation effects*; D001402:B-Lymphocytes / Q000378:metabolism* / Q000528:radiation effects*; D002461:Cell Line, Transformed; D006360:Heat-Shock Proteins / Q000528:radiation effects; D004854:Herpesvirus 4, Human / Q000472:pathogenicity; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis / Q000528:radiation effects; D006358:Hot Temperature / Q000009:adverse effects*; D006801:Humans; D008969:Molecular Sequence Data; D010452:Peptide Biosynthesis; D010455:Peptides / Q000528:radiation effects*; D013744:Tetanus Toxin / Q000378:metabolism / Q000528:radiation effects
D006360:Heat-Shock Proteins; D000949:Histocompatibility Antigens Class II; D010455:Peptides; D013744:Tetanus Toxin