Epitope spreading in immune-mediated diseases: implications for immunotherapy.
Evidence continues to accumulate supporting the hypothesis that tissue damage during an immune response can lead to the priming of self-reactive T and/or B lymphocytes, regardless of the specificity of the initial insult. This review will focus primarily on epitope spreading at the T-cell level. Understanding the cellular and molecular basis of epitope spreading in various chronic immune-mediated human diseases and their animal models is crucial to understanding the pathogenesis of these diseases and to the ultimate goal of designing antigen-specific treatments.
Vanderlugt
Carol L
CL
Department of Microbiology-Immunology, Interdepartmental Immunobiology Center, Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.
Miller
Stephen D
SD
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D000939:Epitopes / Q000276:immunology*; D006084:Graft Rejection / Q000276:immunology / Q000628:therapy; D006801:Humans; D007154:Immune System Diseases / Q000276:immunology* / Q000628:therapy; D007167:Immunotherapy; D009103:Multiple Sclerosis / Q000276:immunology; D009157:Myasthenia Gravis / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology; D014611:Vaccination
D000939:Epitopes