title: Inhibition of atherosclerosis in apoE-null mice by immunization with apoB-100 peptide sequences.
abstract: OBJECTIVE
  LDL oxidation is believed to play an important role in the development of atherosclerosis, and oxidized LDL particles have been shown to become targets for the immune system. Immunization of animals with oxidized LDL results in reduction of atherosclerosis, suggesting an atheroprotective effect of this immune response.
  
  
  RESULTS
  Using a polypeptide library covering the complete sequence of apoB-100, a large number of native and malondialdehyde-modified peptide sequences in apoB-100 that are recognized by antibodies in human plasma were identified. We report here that immunization with apoB-100 peptide sequences, against which high levels of IgG and IgM antibodies are present in healthy human controls, reduce atherosclerosis in apoE-null mice by about 60%. Immunizations with these peptides were also found to increase the collagen content of subvalvular lesions.
  
  
  CONCLUSIONS
  These studies have identified peptide sequences in apoB-100 that induce immune responses, which inhibits atherosclerosis. This suggests a way of developing an immunization therapy for coronary heart disease.
authors.affiliation: Department of Medicine, Malmö University Hospital, Lund University, Malmö, Sweden. Gunilla.Nordin_Fredrikson@medforsk.mas.lu.se
authors.forename: Gunilla Nordin
authors.initials: GN
authors.lastname: Fredrikson
authors.forename: Ingrid
authors.initials: I
authors.lastname: Söderberg
authors.forename: Marie
authors.initials: M
authors.lastname: Lindholm
authors.forename: Paul
authors.initials: P
authors.lastname: Dimayuga
authors.forename: Kuang-Yuh
authors.initials: KY
authors.lastname: Chyu
authors.forename: Prediman K
authors.initials: PK
authors.lastname: Shah
authors.forename: Jan
authors.initials: J
authors.lastname: Nilsson
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D001013:Aorta, Thoracic / Q000737:chemistry / Q000473:pathology; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000737:chemistry / Q000276:immunology*; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D001161:Arteriosclerosis / Q000276:immunology / Q000517:prevention & control*; D001324:Autoantigens / Q000737:chemistry / Q000276:immunology*; D003094:Collagen / Q000032:analysis; D004036:Diet, Atherogenic; D006937:Hypercholesterolemia / Q000235:genetics / Q000276:immunology; D008077:Lipoproteins, LDL / Q000276:immunology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000737:chemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D010446:Peptide Fragments / Q000737:chemistry / Q000276:immunology*; D019151:Peptide Library; D014280:Triglycerides / Q000097:blood
chemical_list: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D001324:Autoantigens; D008077:Lipoproteins, LDL; D010446:Peptide Fragments; D019151:Peptide Library; D014280:Triglycerides; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D003094:Collagen