Inflammation and therapeutic vaccination in CNS diseases

Nature

Volumn 420, Issue 6917, 2002, Pages 879-884

  Weiner, Howard L ^a   Selkoe, Dennis J ^a  

^a Brigham and Women's Hospital Center for Neurologic Diseases   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

IMMUNOLOGY; NEUROLOGY; VACCINES;

CENTRAL NERVOUS SYSTEM; MULTIPLE SCLEROSIS;

DISEASES;

AMYLOID BETA PROTEIN; AUTOANTIGEN; BETA INTERFERON; GLATIRAMER;

MEDICINE;

ALZHEIMER DISEASE; CENTRAL NERVOUS SYSTEM DISEASE; HUMAN; IMMUNE RESPONSE; INFLAMMATION; MULTIPLE SCLEROSIS; NONHUMAN; NUCLEAR MAGNETIC RESONANCE IMAGING; PRIORITY JOURNAL; REVIEW; RISK ASSESSMENT; T LYMPHOCYTE; VACCINATION;

ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN; ANIMALS; ANTIGENS; DISEASE MODELS, ANIMAL; HUMANS; INFLAMMATION; MULTIPLE SCLEROSIS; T-LYMPHOCYTES; VACCINATION; VACCINES;

ANIMALIA;

EID: 0037180823     PISSN: 00280836     EISSN: None     Source Type: Journal    
DOI: 10.1038/nature01325     Document Type: Review

References (67)

1. Prineas, J. W. in Handbook of Multiple Sclerosis (ed. Cook, S. D.) 223-255 (Marcel Dekker, Newark NJ, 1996).
2. Miller, D. H., Grossman, R. I., Reingold, S. C. & McFarland, H. F. The role of magnetic resonance techniques in understanding and managing multiple sclerosis. Brain 121, 3-24 (1998).
3. Weiner, H. L. et al. Serial magnetic resonance imaging in multiple sclerosis: Correlation with attacks, disability, and disease stage. J. Neuroimmunol. 104, 164-173 (2000).
4. Cannella, B. & Raine, C. S. The adhesion molecule and cytokine profile of multiple sclerosis lesions. Ann. Neurol. 37, 424-435 (1995).
5. Sorensen, T. L. et al. Expression of specific chemokines and receptors in the central nervous system of multiple sclerosis patients. J. Clin. Invest. 103, 807-815 (1999).
6. Cuzner, M. L. et al. The expression of tissue-type plasminogen activator, matrix metalloproteases and endogenous inhibitors in the central nervous system in multiple sclerosis: Comparison of stages in lesion evolution. J. Neuropathol. Exp. Neurol. 55, 1194-1204 (1996).
7. Weiner, H. L. A 21 point unifying hypothesis on the etiology and treatment of multiple sclerosis. Can. J. Neurolog. Sci. 25, 93-101 (1998).
8. Cook, S. D., Rohowsky-Kochan, C., Bansil, S. & Dowling, P. C. in Handbook of Multiple Sclerosis (ed. Cook, S. D.) 97-118 (Marcel Dekker, Newark, NJ, 1996).
9. Sibley, W. A., Bamford, C. R. & Clark, K. Clinical viral infections and multiple sclerosis. Lancet 1, 1313-1315 (1985).
10. Edan, G. et al. Therapeutic effect of mitoxantrone combined with methylprednisolone in multiple sclerosis: A randomised multicenter study of active disease using MRI and clinical criteria. J. Neurol. Neurosurg. Psychiat. 62, 112-118 (1997).
11. Gobbini, M. I., Smith, M. E., Richert, N. D., Frank, J. A. & McFarland, H. F. Effect of open label pulse cyclophosphamide therapy on MRI measures of disease activity in five patients with refractory relapsing-remitting multiple sclerosis. J. Neuroimmunol. 99, 142-149 (1999).
12. Weiner, H. L. & Cohen, J. A. Treatment of multiple sclerosis with cylophosphamide: critical review of clinical and immunologic effects. Mult. Scler 8, 142-154 (2002).
13. Goodin, D. S. et al. Disease modifying therapies in multiple sclerosis: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the MS Council for Clinical Practice Guidelines. Neurology 58, 169-178 (2002).
14. Mosmann, T. R. & Sad, S. The expanding universe of T-cell subsets: Th1, Th2, and more. Immunol. Today 17, 138-146 (1996).
15. Maloy, K. J. & Powrie, F. Regulatory T cells in the control of immune pathology. Nature Immunol. 2, 816-822 (2001).
16. Weiner, H. L. Induction and mechanism of action of transforming growth factor-β-secreting Th3 regulatory cells. Immunol. Rev. 182, 207-214 (2001).
17. + T-cell subset inhibits antigen-specifc T-cell responses and prevents colitis. Nture 389, 737-742 (1997).
18. Sakaguchi, S., Sakaguchi, N., Asano, M., Itoh, M. & Tocia, M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor α-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J. Immunol. 155, 1151-1164. (1995).
19. Wucherpfennig, K. W. & Strominger, J. L. Molecular mimicry in T cell-mediated autoimmunity: Viral peptides activate human T cell clones specific for myelin basic protein. Cell 80, 695-705 (1995).
20. Panitch, H. S., Hirsch, R. L., Haley, A. S. & Johnson, K. P. Exacerbations of multiple sclerosis in patients treated with gamma interferon. Lancet 1, 893-895 (1987).
21. + T-cells via CD40 ligand. Proc. Natl Acad. Sci. USA 94, 599-603 (1997).
22. Windhagen, A. et al. Expression of costimulatory molecules B7-1 (CD80), B7-2 (CD86), and interleukin 12 cytokine in multiple sclerosis lesions. J. Exp. Med. 182, 1985-1996 (1995).
23. + T cells via CD40-CD40 ligand interactions. J. Neuroimmunol. 125, 134-140 (2002).
24. + T cells are increased in multiple sclerosis and their ligands MIP-1α and IP-10 are expressed in demyelinating brain lesions. Proc. Natl Acad. Sci. USA 96, 6873-6878 (1999).
25. + monocytes in the blood correlates with the presence of active MRI lesions in MS. J. Neuroimmunol. 119, 145-149 (2001).
26. Comabella, M. et al. Elevated interleukin-12 in progressive multiple sclerosis correlates with disease activity and is normalized by pulse cyclophosphamide therapy. J. Clin. Invest. 102, 671-678 (1998).
27. Chabas, D. et al. The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease. Science 294, 1731-1735 (2001).
28. Iansson, M., Panoutsakopoulou, V., Baker, J., Klein, L. & Cantor, H. Cutting edge: Attenuated experimental autoimmune encephalomyelitis in eta-1/osteopontin-deficient mice. J. Immunol. 168, 2096-2099 (2002).
29. Schenk, D. et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 400, 173-177 (1999).
30. Bard, F. et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nature Med. 6, 916-919 (2000).
31. Becker, K. J. et al. Immunologic tolerance to myelin basic protein decreases stroke size after transient focal cerebral ischemia. Proc. Natl Acad. Sci. USA 94, 10873-10878 (1997).
32. Moalem, G. et al. Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy. Nature Med. 5, 49-55 (1999).
33. Neuhaus, O., Farina, C., Wekerle, H. & Hohlfeld, R. Mechanisms of action of glatiramer acetate in multiple sclerosis. Neurology 56, 702-708 (2001).
34. Olsson, T. et al. Autoreactive T lymphocytes in multiple sclerosis determined by antigen-induced secretion of interferon-γ. J. Clin. Invest. 86, 981-985 (1990).
35. Zhang, J. et al. Increased frequency of IL-2 responsive T-cells specific for myelin basic protein and proteolipid protein in peripheral blood and cerebrospinal fluid of patients with multiple sclerosis. J. Exp. Med. 179, 973-984 (1993).
36. Lehmann, P., Forsthuber, T., Miller, A. & Sercarz, E. Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen. Nature 358, 155-157 (1992).
37. Miller, A., Lider, O. & Weiner, H. L. Antigen-driven bystander suppression following oral administration of antigens. J. Exp. Med. 174, 791-798 (1991).
38. Lafaille, J. J. et al. Myelin basic protein-specific T helper 2 (Th2) cells cause experimental autoimmune encephalomyelitis in immunodeficient hosts rather than protect them from the disease. J. Exp. Med. 186, 307-312 (1997).
39. Romine, J. S. & Salk, J. in Muttiple Sclerosis: Pathology, Diagnosis and Management (eds Hallpike, J. F., Adams, C. M. W. & Tourtelotte, W. W.) 621-630 (Williams & Wilkins, Baltimore, 1983).
40. Bielekova, B. et al Encephalitogenic potential of the myelin basic protein peptide (amino acids 83-99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand. Nature Med. 6, 1167-1175 (2000).
41. Kappos, L. et al. Induction of a non-encephilitogenic type 2 T helper-cell autoimmune response in multiple sclerosis after administration of an altered peptide ligand in a placebo-controlled, randomized phase II trial. The Altered Peptide Ligand in Relapsing MS Study Group. Nature Med. 6, 1176-1182 (2000).
42. Kumar, V., Sercarz, E., Zhang, J. & Cohen, I. T-cell vaccination: From basics to the clinic. Trends Immunol. 22, 539-540 (2001).
43. Vandenbark, A. A. etal. TCR peptide therapy in human autoimmune diseases. Neurochem. Res. 26, 713-730 (2001).
44. Medaer, R., Stinissen, P., Truyen, L., Raus, J. & Zhang, J. Depletion of myelin-basic-protein autoreactive T cells by T-cell vaccination: Pilot trial in multiple sclerosis. Lancet 346, 807-808 (1995).
45. Weissert, R. et al. Protective DNA vaccination against organ-specific autoimmunity is highly specific and discriminates between single amino acid substitutions in the peptide autoantigen. Proc. Natl Acad. Sci. USA 97, 1689-1694 (2000).
46. Wildbaum, G., Westermann, I., Mao, G. & Karin, N. A targeted DNA vaccine encoding fas ligand defines its dual role in the regulation of experimental autoimmune encephalomyelitis. J. Clin. Invest. 106, 671-679 (2000).
47. Wildbaum, G., Netzer, N. & Karin, N. Plasmid DNA encoding IFN-γ-inducible protein 10 redirects antigen-specific T cell polarization and suppresses experimental autoimmune encephalomyelitis. J. Immunol. 168, 5885-5892 (2002).
48. Garren, H. et al. Combination of gene delivery and DNA vaccination to protect from and reverse Th1 autoimmune disease via deviation to the Th2 pathway. Immunity 15, 15-22 (2001).
49. Selkoe, D. J. Alzheimer's disease: Genes, proteins and therapies. Physiol. Rev. 81, 742-761 (2001).
50. Akiyama, H. et al. Inflammation and Alzheimer's disease. Neurobiol. Aging 21, 383-421 (2000).
51. Cooper, N. R., Kalaria, R. N., McGeer, P. L. & Rogers, J. Key issues in Alzheimer's disease inflammation. Neurobiol. Aging 21, 451-453 (2000).
52. McGeer, E. G. & McGeer, P. L. The importance of inflammatory mechanisms in Alzheimer disease. Exp. Gerontol. 33, 371-378 (1998).
53. El Khoury, J., Hickman, S. E., Thomas, C. A., Loike, J. D. & Silverstein, S. C. Microglia, scavenger receptors, and the pathogenesis of Alzheimer's disease. Neurobiol. Aging 19, S81-S84 (1998).
54. Meda, L. et al. Activation of microglial cells by β-amyloid protein and interferon-γ. Nature 374, 647-650 (1995).
55. Wyss-Coray, T. et al. Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice. Proc. Natl Acad. Sci. USA 99, 10837-10842 (2002).
56. Weiner, H. L. et al. Nasal administration of amyloid-β peptide decreases cerebral amyloid burden in mouse model of Alzheimer's disease. Ann. Neurol. 48, 567-579 (2000).
57. Dodart, J. C. et al. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nature Neurosci. 5, 452-457 (2002).
58. DeMattos, R. B. et al. Peripheral anti-Aβ antibody alters CNS and plasma Aβ clearance and decreases brain Aβ burden in a mouse model of Alzheimer's disease. Proc Natl. Acad. Sci. USA 98, 8850-8855 (2001).
59. Schenk, D. in Immunization Against Alzheimer's Disease and Other Neurodegenerative Disorders (eds Selkoe, D. & Christen, Y.) (Springer, Heidelberg, in the press).
60. Furlan, R. et al. Vaccination with amyloid-β peptide induces autoimmune encephalomyelitis in C57BL/6 mice. Brain (in the press).
61. Linington, C., Engelhardt, B., Kapocs, G. & Lassman, H. Induction of persistently demyelinated lesions in the rat following the repeated adoptive transfer ofencephalitogenic T cells and demyelinating antibody. J. Neuroimmunol. 40, 219-224 (1992).
62. McLaurin, J. et al. Therapeutically effective antibodies against amyloid-β peptide target amyloid-β residues 4-10 and inhibit cytotoxicity and fibrillogenesis. Nature Med. 11, 1263-1269 (2002).
63. Monsonego, A., Maron, R., Zota, V., Selkoe, D. J. & Weiner, H. L. Immune hyporesponsiveness to amyloid β-peptide in amyloid precursor protein transgenic mice: Implications for the pathogenesis and treatment of Alzheimer's disease. Proc. Natl Acad. Sci. USA 98, 10273-10278 (2001).
64. Monsonego, A. et al. Immunogenic aspects of amyloid β-peptide: implications for pathogenesis and treatment of Alzheimer's disease. Abstr. no. 423 in Proc. VIII Int. Conf. on Alzheimer's Disease and Related Disorders, Stockholm, Sweden (2002).
65. Trieb, K., Ransmayr, G., Sgonc, R., Lassmann, H. & Grubeck-Loebenstein, B. APP peptides stimulate lymphocyte proliferation in normals, but not in patients with Alzheimer's disease. Neurobiol. Aging 17, 541-547 (1996).
66. Maron, R. et al. Genetic susceptibility or resistance to autoimmune encephalomyelitis in MHC congenic mice is associated with differential production of pro- and anti-inflammatory cytokines. Int. Immunol. 11, 1573-1580 (1999).
67. Wyss-Coray, T. et al. TGF β1 promotes microglial amyloid-beta clearance and reduces plaque burden in transgenic mice. Nature Med. 7, 612-618 (2001).