title: Antigen presenting capacity of brain microvasculature in altered peptide ligand modulation of experimental allergic encephalomyelitis.
abstract: Co-immunization with an altered peptide ligand (LR) partially protects SJL mice from proteolipid protein peptide 139-151-induced experimental allergic encephalomyelitis [Kuchroo, V.K., Greer, J.M., Kaul, D., Ishioka, G.Y., Franco, A., Sette, A., Sobel, R.A., Lees, M.B., 1994. A single TCR antagonist peptide inhibits experimental allergic encephalomyelitis mediated by a diverse T cell repertoire. J. Immunol. 153, 3326-3336; Santambrogio, L., Lees, M.B., Sobel, R.A., 1998. Altered peptide ligand modulation of experimental allergic encephalomyelitis: immune responses within the CNS. J. Neuroimmunol. 81, 1-13]. Clinical protection was noted despite extensive central nervous system inflammation observed after co-immunization with native and altered peptides. To extend our previous reports on this model, we now compare MHC class II expression and antigen presenting cell activity of cells associated with the blood-brain barrier in diseased and protected mice. Immunohistochemical studies identified MHC class II products on both the endothelial and microglial/macrophage populations. Ex vivo experiments suggested a correlation between the reduced clinical disease observed in the co-immunized mice and the antigen presenting activity of cells at the blood-brain barrier. The results suggest that antigen presenting activity is primarily mediated by macrophage-lineage cells of the central nervous system.
authors.affiliation: Biomedical Sciences Division, E.K. Shriver Center, Waltham, MA 02452, USA.
authors.forename: L
authors.initials: L
authors.lastname: Santambrogio
authors.forename: M
authors.initials: M
authors.lastname: Pakaski
authors.forename: M L
authors.initials: ML
authors.lastname: Wong
authors.forename: B
authors.initials: B
authors.lastname: Cipriani
authors.forename: C F
authors.initials: CF
authors.lastname: Brosnan
authors.forename: M B
authors.initials: MB
authors.lastname: Lees
authors.forename: M E
authors.initials: ME
authors.lastname: Dorf
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D001812:Blood-Brain Barrier / Q000276:immunology; D001921:Brain / Q000098:blood supply / Q000166:cytology / Q000276:immunology*; D002460:Cell Line; D002560:Cerebrovascular Circulation / Q000276:immunology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis / Q000096:biosynthesis; D007114:Immunization; D008024:Ligands; D016177:Macrophage-1 Antigen / Q000032:analysis; D008264:Macrophages / Q000737:chemistry / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D008833:Microcirculation / Q000276:immunology; D017628:Microglia / Q000737:chemistry / Q000276:immunology / Q000378:metabolism; D018991:Myelin Proteolipid Protein / Q000276:immunology / Q000494:pharmacology; D009474:Neurons / Q000737:chemistry / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000949:Histocompatibility Antigens Class II; D008024:Ligands; D016177:Macrophage-1 Antigen; D018991:Myelin Proteolipid Protein; D010446:Peptide Fragments; C435023:myelin proteolipid protein (139-151)