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MULTİPL SKLEROZUN İMMÜNOPATOLOJİSİ

Immunopathology of multiple sclerosis

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Abstract (2. Language): 
Aim: Multiple sclerosis (MS) is an immune- mediated disease of the central nervous system. We will emphasize in this article; very different mechanisms, and complex interactions have important role in immunopathology of multiple sclerosis. Main Findings: The pathogenesis of MS is best viewed as a complex interaction between genetically predetermined susceptibility markers and environmen¬tal stimuli. MS is charecterized by inflammation, demyelination, apoptosis in oligodendrocytes, rem-yelination, and axon loss. Immune reaction against different components of the central nervous sys¬tem (particularly myelin structures) are thought to play an important role in the initiation of the dest¬ructive process. The inflammation in MS appears to be caused by an overactive pro-inflammatory TH1 profile in T cells. Demyelination can result as a consequence of direct damage to myelin by inf¬lammatory cells or indirectly because of the enviroment produced by inflammation. /Axon loss occurs in MS lesions starting early in the disease. Conclusion: MS occurs with different immünopat-hological mechanisms.
Abstract (Original Language): 
Amaç: Multipl skleroz (MS) santral sinir sisteminin (SSS) immün aracılı hastalığıdır. Biz bu makalede MS'nin immünopatolojisinde çok farklı mekanizmalar ve kompleks etkileşimlerin önemli role sahip ol¬duğunu vurgulayacağız. Ana Bulgular: MS'nin patogenezi çevresel uyaran ve genetik olarak yat¬kınlık arasında kompleks etkileşimin en iyi görünümüdür. MS inflamasyon, demiyelinizasyon, oligo-dendrosit apopitozu, remiyelinizasyon ve akson kaybıyla karekterizedir. SSS'nin farklı komponentleri-ne (miyelin striktürleri) karşı immün reaksiyon destrüktif proçesin başlamasında önemli role sahiptir. MS'de inflamasyon proinflamatuvar TH1 profilinde T hücrelerinin sayesindedir. Demiyelinzasyon, inf-lamasyonla oluşan çevrenin indirekt etkisi veya inflamatuvar hücrelerce miyelinin direkt hasarı netice¬sinde gelişebilir. Akson kaybı, hastalıkta MS lezyonlarının erken başlangıcında görülür. Sonuç: MS farklı immünopatolojik mekanizmalarla gelişir.
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REFERENCES

References: 

1. Ge Y, Grossman RI, Udupa JK. Magnetization trans-fer ratio histogram analysis of normal appearing gray matter and normal appearing white matter in multiple sclerosis. J Comput Asist Tomogr 2002; 26(1): 62-8
2. Sospedra M, Martin R. Immunology of multiple scle¬rosis. Annu Rev immunol 2005; 23: 683- 747
3. Alexandre P, Jack A. Pathogenesis of multiple sclero¬sis. Curr Opin Neurol 2005; 18: 225- 30
4. Edward J.Fox. Immunolopathology of multiple scle¬rosis. Neurology 2004; 63(6): 3-7
5. Lassmann H, Bruck W, Lucchinetti C. Heterogeneity of multiple sclerosis pathogenesis implications for diag¬nosis and therapy. Trends Mol Med 2001; 7: 115- 21
6. Lassmann H. Mechanisms of demyelination and tis¬sue destruction in multiple sclerosis. Clin Neurol Ne-
urosurg 2002; 104: 168- 71
7. Lucchinetti C, Bruck W, Parisi J. Implications for the pathogenesis of demyelination. Ann Neurol 2000; 47:
707- 17
8. Zhou D, Hemmer B. Specificity and degeneracy: T cell recognition in CNS autoimmunity. Mol immunol
2004; 40: 2428- 33
9. Hemmer B, Vergelli M, Tranquill L, Conlon P, Ling N, McFarland HF, Martin R. Human T-cell response to myelin basic protein peptide (83-99): extensive hetero¬geneity in antigen recognition, function, and phenoty-pe. Neurology 1997; 49(4): 1116- 26
10. Kim HJ, Antel JP, Duquette P. Persisitence of immu-
ne responses to altered and native myelin antigens in
patients with multiple sclerosis treated with altered
peptide ligand. Clin Immunol 2002; 104: 105- 14
11. idlman E. Santral sinir sisteminin mlyelln hastalıkla¬rı: Oğul E; ed. Klinik Nöroloji. Birinci baskı. istanbul: No¬bel & Güneş Tıp Kltabevl; 2002: 159- 70
12. Comabella M, Balashov K, Issazadeh S, Smith D, Weiner HL, Khoury SJ. Elevated lnterleukln-12 in prog¬ressive multiple sclerosis correlates with disease activity and is normalized by pulse cyclophosphamide the¬rapy. J Clin Invest 1998; 102(4): 671- 8
13. Chltnls T, Khoury SJ. Neurolmmunology. In: Brad¬ley WG, Daroff RB, Fenlchel GM, Jankovlc J; eds. Ne¬urology in clinical practice. 4nd ed. Philadelphia: But¬terworth Heinemann; 2004: 823- 5
14. Nakajlma H, Fukuda K, Dol Y, Suglno M, Klmura F, Hanafusa T, Ikemoto T, Shlmlzu A. Expression of TH1/TH2-related chemoklne receptors on peripheral T cells and correlation with clinical disease activity in pa¬tients with multiple sclerosis. Eur Neurol 2004; 52(3):
162-8
15. Torres BA, Komlnsky S, Perrln GQ, Hobelka AC, Johnson HM. Superantigens: the good, the bad, and the ugly. Exp Biol Med (Maywood) 2001; 226(3): 164¬76
16. Mlnagar A, Alexander JS. Blood-brain barrier dis¬ruption in multiple sclerosis. Mult Scler 2003; 9(6): 540¬9
17. Cannella B, Raine CS. The adhesion molecule and cytokine profile of multiple sclerosis lesions. Ann Ne-
urol 1995; 37(4): 424- 35
18. Glmenez MA, Sim JE, Russell JH. TNFR1-dependent VCAM-1 expression by astrocytes exposes the CNS to destructive inflammation. J Neurolmmunol 2004; 151(1-2): 116- 25

19. Sellebjerg F, Sorensen TL Chemokines and matrix metalloproteinase-9 in leukocyte recruitment to the central nervous system. Brain Res Bull 2003; 61(3):
347- 55
20. Abraham M, Shapiro S, Karni A, Weiner HL, Miller A. Gelatinases (MMP-2 and MMP-9) are preferentially expressed by Th1 vs. Th2 cells. J Neuroimmunol 2005;
163(1-2): 157-64
21. Avolio C, Filippi M, Tortorella C, Rocca MA, Ruggi-eri M, Agosta F, Tomassini V, Pozzilli C, Stecchi S, Gi-aquinto P, Livrea P, Trojano M. Serum MMP-9/TIMP-1 and MMP-2/TIMP-2 ratios in multiple sclerosis: relati¬onships with different magnetic resonance imaging measures of disease activity during IFN-beta-1a treat¬ment. Mult Scler 2005; 11(4): 441- 6
22. Kanesaka T, Mori M, Hattori T, Oki T, Kuwabara S. Serum matrix metalloproteinase-3 levels correlate with disease activity in relapsing-remitting multiple sclerosis. J Neurol Neurosurg Psychiatry 2006; 77(2): 185- 8
23. Dal Canto MC, Melvold RW, Kim BS, Miller SD. Two
models of multiple sclerosis: experimental allergic en-cephalomyelitis (EAE) and Theiler's murine encepha-lomyelitis virus (TMEV) infection. A pathological and immunological comparison. Microsc Res Tech 1995;
32(3): 215- 29
24. Tuohy VK, Kinkel RP. Epitope spreading: a mecha-nism for progression of autoimmune disease. Arch Im¬munol Ther Exp (Warsz) 2000;48(5):347- 51
25. Wekerle H, Kojima K, Lannes-Vieira J, Lassmann H, Linington C. Animal models. Ann Neurol 1994; 36 Suppl: S47- 53
26. Soos JM, Mujtaba MG, Schiffenbauer J, Torres BA, Johnson HM. Intramolecular epitope spreading indu-ced by staphylococcal enterotoxin superantigen reacti¬vation of experimental allergic encephalomyelitis. J Ne-
uroimmunol 2002; 123(1- 2): 30- 4
27. Von Budingen HC, Tanuma N, Villoslada P, Oual-let JC, Hauser SL, Genain CP. Immune responses aga¬inst the myelin/oligodendrocyte glycoprotein in expe¬rimental autoimmune demyelination. J Clin Immunol
2001; 21(3): 155- 70
28. Hendriks JJ, Teunissen CE, de Vries HE, Dijkstra CD. Macrophages and neurodegeneration. Brain Res
Rev 2005; 48(2): 185- 95
29. Furlan R, Rovaris M, Martinelli Boneschi F, Khade-mi M, Bergami A, Gironi M, Deleidi M, Agosta F, Fran-ciotta D, Scarpini E, Uccelli A, Zaffaroni M, Kurne A, Co¬mi G, Olsson T, Filippi M, Martino G. Immunological patterns identifying disease course and evolution in multiple sclerosis patients. J Neuroimmunol 2005;
165(1-2): 192- 200
30. Jurewicz A, Matysiak M, Tybor K, Kilianek L, Raine CS, Selmaj K. Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apopto-
sis inducing factor. Brain 2005; 128(Pt 11): 2675- 88
31. Rieckmann P. Neurodegeneration and clinical rele¬vance for early treatment in multiple sclerosis. Int MS J
2005; 12(2): 42- 51
32. Gao YL, Brosnan CF, Raine CS. Experimental auto¬immune encephalomyelitis. Qualitative and semiquan¬titative differences in heat shock protein 60 expression in the central nervous system. J Immunol 1995 Apr 1;154(7):3548- 56
33. Trapp BD, Peterson J, Ransohott R. Axonal trans-section in the lesions of multiple sclerosis. New Eng J
Med 1998; 338: 278- 85
34. Como L. Neuroprotection in multiple sclerosis. MS forum Mach 2004 Workshop
35. Bjartmar C, Kinkel RP, Kidd G. Axonal loss in nor-mal-appearing white matter in a patient with acute
MS. Neurol 2001; 57: 1248- 52
36. Stys PK. General mechanisms of axonal damage and its prevention. J Neurol Sci 2005; 233(1-2): 3- 13
37. Nakanishi H. Microglial functions and proteases.
Mol Neurobiol 2003; 27(2): 163- 76
38. Miller DH, Barkhof F, Frank JA, Parker GJ, Thomp-son AJ. Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical
relevance. Brain 2002; 125: 1676- 95
39. Kuhlmann T, Lingfeld G, Bitsch A, Schuchardt J, Bruck W. Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases
over time. Brain 2002; 125: 2202- 12
40. Bruck W. Inflammatory demyelination is not cent-ral to the pathogenesis of multiple sclerosis. J Neurol
2005; 252 Suppl 5:v10-5
41. Pagani E, Rocca MA, Gallo A. Regional brain at-rophy evolves differantly in MS patients according to their clinical phenotypes. Neurology 2004; 62(suppl
5): A287- 8
42. Minagar A, Toledo EG, Alexander JS, Kelley RE. Pat-hogenesis of brain and spinal cord atrophy in multiple sclerosis. J Neuroimaging 2004; 14(3 Suppl): 5-10
43. Lucchinetti C, Bruck W, Parisi J. Heterogeneity of multiple sclerosis lesions: implications for the pat-hogenesis of demyelination. Ann Neurol 2000; 47:
707- 17
44. Barnett MH, Prineas JW. Relapsing and remitting multiple sclerosis: pathology of the newly forming
lesion. Ann Neurol 2004; 55: 458- 68

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