title: A role for the heat shock protein-CD91 axis in the initiation of immune responses to tumors.
abstract: For over 100 years, it has been established that tumor-specific immune responses can frequently be detected in the tumor-bearing host. Whether or not these immune responses are capable of controlling the growth of the tumor is influenced by many factors. However, the mechanism by which the immune responses are initiated in the first place has remained a dilemma. In this chapter, we present evidence that heat shock protein-peptide complexes released by tumor cells are the entity responsible for initiating the immune responses. Interaction of the extracellular HSP with its receptor CD91 is necessary for priming the immune response. We propose that the disruption of the HSP-CD91 interaction may be an active mechanism by which tumors prevent the generation of immune responses against it.
authors: Department of Immunology, University of Pittsburgh, E1051, BSTWR, 200 Lothrop Street, Pittsburgh, PA 15261, USA.
authors: Sudesh
authors: S
authors: Pawaria
authors: Michelle Nicole
authors: MN
authors: Messmer
authors: Yu Jerry
authors: YJ
authors: Zhou
authors: Robert Julian
authors: RJ
authors: Binder
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D006360:Heat-Shock Proteins / Q000276:immunology* / Q000378:metabolism*; D006801:Humans; D026503:Low Density Lipoprotein Receptor-Related Protein-1 / Q000276:immunology* / Q000378:metabolism*; D009369:Neoplasms / Q000276:immunology*; D011485:Protein Binding / Q000502:physiology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D006360:Heat-Shock Proteins; D026503:Low Density Lipoprotein Receptor-Related Protein-1