The CD4-Th1 model for multiple sclerosis: A crucial re-appraisal

Trends in Immunology

Volumn 25, Issue 3, 2004, Pages 132-137

  Lassmann, Hans ^a   Ransohoff, Richard M ^b  

^a MEDICAL UNIVERSITY OF VIENNA   (Austria)

^b LERNER RESEARCH INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CD4 ANTIGEN; CYTOKINE; GAMMA INTERFERON; MYELIN; TUMOR NECROSIS FACTOR ALPHA;

AUTOIMMUNITY; CENTRAL NERVOUS SYSTEM DISEASE; CLINICAL FEATURE; DEMYELINATING DISEASE; DISEASE COURSE; EXPERIMENTAL MODEL; MULTIPLE SCLEROSIS; NEUROPATHOLOGY; NONHUMAN; PREDICTION; REVIEW; SYMPTOM; T LYMPHOCYTE; TH1 CELL;

EID: 1342345214     PISSN: 14714906     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.it.2004.01.007     Document Type: Article

References (57)

1. Noseworthy J.H., et al. Multiple sclerosis. N. Engl. J. Med. 343:2000;938-952.
2. Herrera B.M., Ebers G.C. Progress in deciphering the genetics of multiple sclerosis. Curr. Opin. Neurol. 16:2003;253-258.
3. + T cells: evidence for trafficking through choroids plexus and meningen via P-selectin. Proc. Natl. Acad. Sci. U. S. A. 100:2003;8389-8394.
4. Lassmann H. Comparative neuropathology of chronic experimental allergic encephalomyelitis and multiple sclerosis. Schriftenr. Neurol. 25:1983;1-135.
5. Huang D., et al. Chemokines and chemokine receptors in inflammation of the nervous system: manifold roles and exquisite regulation. Immunol. Rev. 177:2000;52-67.
6. Krogsgaard M., et al. Visualization of myelin basic protein (MBP) T cell epitopes in multiple sclerosis lesions using a monoclonal antibody specific for the human histocompatibility leukocyte antigen (HLA)-DR2-MBP 85-99 complex. J. Exp. Med. 191:2000;1395-1412.
7. Oksenberg J.R., et al. Selection for T-cell receptor Vβ-Dβ- Jβ gene rearrangements with specificity for a myelin basic protein peptide in brain lesions of multiple sclerosis. Nature. 362:1993;68-70.
8. Hohlfeld R. Biotechnological agents for the immunotherapy of multiple sclerosis. Principles, problems and persectives. Brain. 120:1997;865-916.
9. Booss J., et al. Immunohistological analysis of T lymphocyte subsets in the central nervous system in chronic progressive multiple sclerosis. J. Neurol. Sci. 62:1983;219-232.
10. Gay F.W., et al. The application of multifactorial cluster analysis in the staging of plaques in early multiple sclerosis: Identification and characterization of the primary demyelinating lesion. Brain. 120:1997;1461-1483.
11. + T cells dominate the T cell infiltrate in active multiple sclerosis lesions as shown by micromanipulation and single cell polymerase chain reaction. J. Exp. Med. 192:2000;393-404.
12. Rivera-Quiñones C., et al. Absence of neurological deficits following extensive demyelination in a class I-deficient murine model of multiple sclerosis. Nat. Med. 4:1998;187-193.
13. + T-cells in a model for multiple sclerosis. J. Exp. Med. 194:2001;669-676.
14. + T cells are encephalitogenic and produce severe disease in C57BL/6 mice. J. Immunol. 166:2001;7579-7587.
15. Cabarrocas J., et al. Effective and selective immune surveillance of the brain by MHC class I-restricted cytotoxic T lymphocytes. Eur. J. Immunol. 33:2003;1174-1182.
16. -/- mice. Science. 256:1992;1210-1213.
17. Höftberger, R. et al. Expression of major histocompatibiltiy complex class i molecules on the different cell types in multiple sclerosis lesions. Brain Pathol. (in press).
18. Neumann H., et al. Cytotoxic T lymphocytes in autoimmune and degenerative CNS diseases. Trends Neurosci. 25:2002;313-319.
19. Flugel A., et al. Migratory activity and functional changes of green fluorescent effector cells before and during experiemntal autoimmune encephalomyelitis. Immunity. 14:2001;547-560.
20. Moalem G., et al. Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy. Nat. Med. 5:1999;49-55.
21. Kerschensteiner M., et al. Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation? J. Exp. Med. 189:1999;865-870.
22. Stadelmann C., et al. BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective interactions between immune cells and neuronal cells? Brain. 125:2002;75-85.
23. Lafaille J.J., et al. High incidence of spontaneous autoimmune encephalomyelitis in immunodeficient anti-myelin basic protein T cell receptor transgenic mice. Cell. 78:1994;399-408.
24. Ottenhoff T.H., et al. Genetics, cytokines and human infectious disease: lessons from weakly pathogenic mycobacteria and salmonellae. Nat. Genet. 32:2002;97-105.
25. Gomez-Reino J.J., et al. Treatment of rheumatoid arthritis with tumor necrosis factor inhibitors may predispose to significant increase in tuberculosis risk: a multicenter active-surveillance report. Arthritis Rheum. 48:2003;2122-2127.
26. Duong T.T., et al. Effect of anti-interferon-γ and anti-interleukin-2 monoclonal antibody treatment on the development of actively and passively induced experimental allergic encephalomyelitis in the SJL/J mouse. J. Neuroimmunol. 36:1992;105-115.
27. Ferber I.A., et al. Mice with a disrupted IFN-γ gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J. Immunol. 156:1996;5-7.
28. Chu C.Q., et al. Failure to suppress the expansion of the activated CD4 T cell population in interferon γ-deficient mice leads to exacerbation of experimental autoimmune encephalomyelitis. J. Exp. Med. 192:2000;123-128.
29. Furlan R., et al. Intrathecal delivery of IFN-γ protects C57BL/6 mice from chronic-progressive experimental autoimmune encephalomyelitis by increasing apoptosis of central nervous system-infiltrating lymphocytes. J. Immunol. 167:2001;1821-1829.
30. Willenborg D.O., et al. IFN-γ is critical to the control of murine autoimmune encephalomyelitis and regulates both in the periphery and in the target tissue: a possible role for nitric oxide. J. Immunol. 163:1999;5278-5286.
31. + myelopoiesis induced by CFA: a clue to the paradoxical effects of IFN-γ in autoimmune disease models. Trends Immunol. 22:2001;367-371.
32. Panitch H.S., et al. Treatment of multiple sclerosis with γ interferon: exacerbations associated with activation of the immune system. Neurology. 37:1987;1097-1102.
33. TNF neutralization in MS: results of a randomized, placebo-controlled multicenter study. Neurology. 53:1999;457-465.
34. Probert L., et al. TNFR1 signalling is critical for the development of demyelination and the limitation of T-cell responses during immune mediated CNS disease. Brain. 123:2000;2005-2019.
35. Mohan N., et al. Demyelination occurring during anti-tumor necrosis factor α therapy for inflammatory arthritides. Arthritis Rheum. 44:2001;2862-2869.
36. Kuchroo V.K. T-cell response in experimental autoimmune encephalomyelitis (EAE): role of self and cross-reactive antigens in shaping, tuning, and regulating the autopathogenic T cell repertoire. Annu. Rev. Immunol. 20:2002;101-123.
37. 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 disease. J. Exp. Med. 186:1997;307-312.
38. Storch M.K., et al. Autoimmunity to myelin oligodendrocyte glycoprotein in rats mimics the spectrum of multiple sclerosis pathology. Brain Pathol. 8:1998;681-694.
39. Stefferl A., et al. Myelin oligodendrocyte glycoprotein induces experimental autoimmune encephalomyelitis in the resistant Brown Norway rat: disease susceptibility is determined by MHC and MHC-linked effects on the B-cell response. J. Immunol. 163:1999;40-49.
40. Lucchinetti C.F., et al. A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica. Brain. 125:2002;1450-1461.
41. Lucchinetti C., et al. Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination. Ann. Neurol. 47:2000;707-717.
42. Lassmann H. Pathology of multiple sclerosis. Compston A. McAlpine's Multiple Sclerosis. 1998;323-358 Churchill Liningstone, London.
43. Ferguson B., et al. Axonal damage in acute multiple sclerosis lesions. Brain. 120:1997;393-399.
44. Trapp B.D., et al. Axonal transection in the lesions of multiple sclerosis. N. Engl. J. Med. 338:1998;278-285.
45. Bjartmar C., et al. Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the disease. J. Neurol. Sci. 206:2003;165-171.
46. Ganter P., et al. Spinal cord axonal loss in multiple sclerosis: a post-mortem study. Neuropathol. Appl. Neurobiol. 25:1999;459-467.
47. Evangelou N., et al. Regional axonal loss in the corpus callosum correlates with cerebral white matter lesion volume and distribution in multiple sclerosis. Brain. 123:2000;1845-1849.
48. Filippi M., et al. Evidence for widespread axonal damage at the earliest clinical stage of multiple sclerosis. Brain. 126:2003;433-437.
49. Bozzali M., et al. Quantification of brain grey matter damage in different MS phenotypes by use of diffusion tensor MR imaging. AJNR Am. J. Neuroradiol. 23:2002;985-988.
50. Owens T. The enigma of multiple sclerosis: inflammation and neurodegeneration causes heterogenous dysfunction and damage. Curr. Opin. Neurol. 16:2003;259-265.
51. Zamvil S.S., Steinman L. Diverse targets for intervention during inflammatory and neurodegenerative phases of multiple sclerosis. Neuron. 38:2003;685-688.
52. Leary S.M., Thompson A.J. Treatment for patients with primary progressive multiple sclerosis. Cohen J.A., Rudick R.A. Multiple Sclerosis Therapeutics. 2003;589-598 Martin Dunitz, London.
53. Filippi M., et al. Comparison of triple dose versus standard dose gadolinium-DTPA for detection of MRI enhancing lesions in patients with primary progressive multiple sclerosis. J. Neurol. Neurosurg. Psychiatry. 59:1995;540-544.
54. Filippi M. MRI-clinical correlations in the primary progressive course of MS: new insights into the disease pathophysiology from the application of magnetization transfer, diffusion tensor, and functional MRI. J. Neurol. Sci. 206:2003;157-164.
55. Storch M.K., et al. Multiple sclerosis: in situ evidence for antibody and complement mediated demyelination. Ann. Neurol. 43:1998;465-471.
56. Aboul-Enein F., et al. Preferential loss of myelin associated glycoprotein reflects hypoxia-like white matter damage in stroke and inflammatory brain diseases. J. Neuropathol. Exp. Neurol. 62:2003;25-33.
57. Lucchinetti C., et al. Distinct patterns of multiple sclerosis pathology indicates heterogeneity in pathogenesis. Brain Pathol. 6:1996;259-274.