Heat-shock proteins and the host-pathogen interaction during bacterial infection.
Heat-shock proteins (HSPs) are expressed at high levels by bacterial pathogens during adaptation to intracellular survival. Both host and pathogen heat-shock proteins contribute to immunity by receptor-mediated activation of the innate immune response and by participation in the presentation of antigens for the adaptive immune response. Manipulation of these interactions presents a potential route to improved control of infection by vaccination or immunotherapy.
Stewart
Graham R
GR
Department of Infectious Diseases and Microbiology, Centre for Molecular Microbiology and Infection, Imperial College London, South Kensington Campus, London SW7 2AZ, UK. g.stewart@imperial.ac.uk
Young
Douglas B
DB
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology; D001419:Bacteria / Q000276:immunology*; D001424:Bacterial Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006360:Heat-Shock Proteins / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D008562:Membrane Glycoproteins / Q000276:immunology; D051379:Mice; D011956:Receptors, Cell Surface / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D051193:Toll-Like Receptors
D015703:Antigens, CD; D006360:Heat-Shock Proteins; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors