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Новые сигнальные молекулы в патогенезе аутоиммунных заболеванийъ
УДК:
616.092
Автор статьи:
Ильясова Б.С.
Место работы автора:
Научно-исследовательский институт кардиологии и внутренних болезней МЗ РК
Название журнала:
Гигиена, эпидемиология и иммунобиология
Год выпуска:
2010
Номер журнала:
1(43)
Страницы:
с.161-165
Ключевые слова:
аутоиммунные заболевания, интерлейкин, цитокины
Резюме на казахском языке:
Мақала 17 типті Т-хелперлер және ИЛ-17, ИЛ-18 интерлейкиндерінің аутоиммунды қабыну басталуында қатысуы туралы қазіргі заманғы ұсыныстарға арналған. Т-хелперлер субпопуляциясы активациясы немесе супрессиясы цитокиндер әрекеті арқасында аутоиммунды немесе аллергиялық аурулар дамуын анықтайтын Тh1-, Th2-, Th17- и Treg- лимфоциттерімен ұсынылған.
Резюме на английском языке:
In this paper is described about modern statement of the participation of T-helpers of 1 type and interleukins of IL-17, IL-23, IL-18, Il-21 in the initiation of autoimmune inflammation. Subsets of the T-helpers are Тh1-, Th2-, Th17- и Treglymphocytes, are activated or are suppressed by cytokins action and determinates the development of the autoimmune or allergic diseases.
Список литературы:
1. Mossman T. R., Chervinski H., Bond M. W. et all. Two types of mutine helper T-cell clon. I. Definition according the profiles of lynphokine activitiesand secreted proteins. J. Immunology. 136: 2348-2357.
2. Coffman R. L. Origins of the Th1-Th2 model, personal perspective. Nature Immunology, 2006. 7. Р. 539-541.
3. Ilona Catcher, Burkhard Becher. The J. of Clinical Investigation. Vol 117, N5, 2007, P1119-1127.
4. Yoshimoto T., et al. IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, and B-cells: synergism with Il-18 for INF-gamma production. J. Immunolog. 161. Р. 3400-3407, 1998.
5. Racke m. K., et al. Cytokin-induced immune deviation as a therapy for inflammatory autoimmune diseases. J. Exp. Med., 1994, 180, P. 1113-1119.
6. Ferber I. A., et al. Mice with the disrupted INF-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J. Immunology, 1996, 156: P. 5-7.
7. Frei K., et al Tumor necrosis factor alpha are notrequired for induction of acute experimental autoimmune encephalomyelitis. J. Exp. Med., 185: P. 2177-2182.
8. Oppman B. Et al. 2000. Novel p19 protein engangesIl-12p40 to form a cytokine, IL-23, with biologicalactivities similar as well as disnictfrom IL-12. Immunity, 2000. 13. P. 715-725.
9. Langrish C. L., ey al. IL-23 drives a pathogenic T-cell population that induces autoimmune inflammation. J. Exp. Med. 2005, 201, P. 233-240.
10. Kennedy J. Et al. 1996. Mouse IL-17. cytokine preferencially expressed by alpha beta TCR+CD4-CD8-T-cells. J. Interferon Cytokine Res. 1996, 16, P: 611-617.
11. Aggarval S. Et Gurney A. L. Il-17 prototype member of an emerging cytokines family. J. Leukoc. Biol., 2002, 71. P. 1-8.
12. Gaffen S. L. Kramer J. M. Yu J. J. and Shen F. The Il-17 cytokine family. Vitam. Horm, 74, P. 255-282.
13. Chabaut M. et al. Human intarleukine-17: a T-cell derived proinflammatory cytokine produced by rheumatoid synoviun. Artritis Rheum. 1999. 42. P. 963-970.
14. Matusevicius D., et al. Interleukine-17 mRNA expression in blood and CSF mononuclear cells is augmentedin multiple sclerosis. Mult Scl. 5 P. 101-104.
15. Kastelein RA, Hunter CA, Cua DJ. Discoveryand biology of IL-23 and IL-27: related but functionally distinct regulators of inflammation. Annu Rev Immunol2007. 25: 221–242. Oppmann B, Lesley R, Blom B, Timans JC.
16. Xu Y, Hunte B et al. Novel p19 protein engagesIL-12p 40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity2000. 13: 715–725.
17. Yang XO, Panopoulos AD, Nurieva R, ChangSH, Wang D, Watowich SS et al. STAT3 regulates cytokine-mediated generation of inflammatory helper Tcells. J Biol Chem 2007. 282: 9358–9363.
18. Ivanov II, McKenzie BS, Zhou L, TadokoroCE, Lepelley A, Lafaille JJ et al. The orphan nuclear receptor RORgammat directs the differentiation programof proinflammatory IL-17+ T helper cells. Cell 2006. 126: 1121–1133.
19. Dinarello CA. Interleukin-18 and the pathogenesis of inflammatory diseases. Semin Nephrol. 2007Jan. 27 (1): 98-114.
20. Harrington LE, et all, 2006;
21. Weaver CT, et all, 2006.
22. Korn T, Bettelli E, Gao W, Awasthi A, Jager A, Strom TB et al. IL-21 initiates an alternative pathway toinduce proinflammatory T (H) 17 cells. Nature 2007. 448: 484–487. |
23. Nurieva R, Yang XO, Martinez G, Zhang Y, Panopoulos AD, Ma L et al. Essential autocrine regulationby IL-21 in the generation of inflammatory T cells. Nature2007. 448: 480–483.
24. Zhou L, Ivanov II, Spolski R, Min R, Shenderov K, Egawa T et al. IL-6 programs T (H) -17 cell differentiation by promoting sequential engagement of the IL-21 andIL-23 pathways. Nat Immunol 2007. doi: 10. 1038/ni1488.
25. Leonard WJ, Spolski R. Interleukin-21: amodulator of lymphoid proliferation, apoptosis and differentiation. Nat Rev Immunol 2005. 5: 688–698.
1. Mossman T. R., Chervinski H., Bond M. W. et all. Two types of mutine helper T-cell clon. I. Definition according the profiles of lynphokine activitiesand secreted proteins. J. Immunology. 136: 2348-2357.
2. Coffman R. L. Origins of the Th1-Th2 model, personal perspective. Nature Immunology, 2006. 7. Р. 539-541.
3. Ilona Catcher, Burkhard Becher. The J. of Clinical Investigation. Vol 117, N5, 2007, P1119-1127.
4. Yoshimoto T., et al. IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, and B-cells: synergism with Il-18 for INF-gamma production. J. Immunolog. 161. Р. 3400-3407, 1998.
5. Racke m. K., et al. Cytokin-induced immune deviation as a therapy for inflammatory autoimmune diseases. J. Exp. Med., 1994, 180, P. 1113-1119.
6. Ferber I. A., et al. Mice with the disrupted INF-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J. Immunology, 1996, 156: P. 5-7.
7. Frei K., et al Tumor necrosis factor alpha are notrequired for induction of acute experimental autoimmune encephalomyelitis. J. Exp. Med., 185: P. 2177-2182.
8. Oppman B. Et al. 2000. Novel p19 protein engangesIl-12p40 to form a cytokine, IL-23, with biologicalactivities similar as well as disnictfrom IL-12. Immunity, 2000. 13. P. 715-725.
9. Langrish C. L., ey al. IL-23 drives a pathogenic T-cell population that induces autoimmune inflammation. J. Exp. Med. 2005, 201, P. 233-240.
10. Kennedy J. Et al. 1996. Mouse IL-17. cytokine preferencially expressed by alpha beta TCR+CD4-CD8-T-cells. J. Interferon Cytokine Res. 1996, 16, P: 611-617.
11. Aggarval S. Et Gurney A. L. Il-17 prototype member of an emerging cytokines family. J. Leukoc. Biol., 2002, 71. P. 1-8.
12. Gaffen S. L. Kramer J. M. Yu J. J. and Shen F. The Il-17 cytokine family. Vitam. Horm, 74, P. 255-282.
13. Chabaut M. et al. Human intarleukine-17: a T-cell derived proinflammatory cytokine produced by rheumatoid synoviun. Artritis Rheum. 1999. 42. P. 963-970.
14. Matusevicius D., et al. Interleukine-17 mRNA expression in blood and CSF mononuclear cells is augmentedin multiple sclerosis. Mult Scl. 5 P. 101-104.
15. Kastelein RA, Hunter CA, Cua DJ. Discoveryand biology of IL-23 and IL-27: related but functionally distinct regulators of inflammation. Annu Rev Immunol2007. 25: 221–242. Oppmann B, Lesley R, Blom B, Timans JC.
16. Xu Y, Hunte B et al. Novel p19 protein engagesIL-12p 40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity2000. 13: 715–725.
17. Yang XO, Panopoulos AD, Nurieva R, ChangSH, Wang D, Watowich SS et al. STAT3 regulates cytokine-mediated generation of inflammatory helper Tcells. J Biol Chem 2007. 282: 9358–9363.
18. Ivanov II, McKenzie BS, Zhou L, TadokoroCE, Lepelley A, Lafaille JJ et al. The orphan nuclear receptor RORgammat directs the differentiation programof proinflammatory IL-17+ T helper cells. Cell 2006. 126: 1121–1133.
19. Dinarello CA. Interleukin-18 and the pathogenesis of inflammatory diseases. Semin Nephrol. 2007Jan. 27 (1): 98-114.
20. Harrington LE, et all, 2006;
21. Weaver CT, et all, 2006.
22. Korn T, Bettelli E, Gao W, Awasthi A, Jager A, Strom TB et al. IL-21 initiates an alternative pathway toinduce proinflammatory T (H) 17 cells. Nature 2007. 448: 484–487. |
23. Nurieva R, Yang XO, Martinez G, Zhang Y, Panopoulos AD, Ma L et al. Essential autocrine regulationby IL-21 in the generation of inflammatory T cells. Nature2007. 448: 480–483.
24. Zhou L, Ivanov II, Spolski R, Min R, Shenderov K, Egawa T et al. IL-6 programs T (H) -17 cell differentiation by promoting sequential engagement of the IL-21 andIL-23 pathways. Nat Immunol 2007. doi: 10. 1038/ni1488.
25. Leonard WJ, Spolski R. Interleukin-21: amodulator of lymphoid proliferation, apoptosis and differentiation. Nat Rev Immunol 2005. 5: 688–698.
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Статья посвящена современным представлениям об участии Т-хелперов 17 типа и интерлейкинов ИЛ-17, ИЛ-23, ИЛ-18, ИЛ-21 в запуске аутоиммунного воспаления. Субпопуляции Т-хелперов представлены Тh1-, Th2-, Th17- и Treg-лимфоцитами, активация или супрессия которых под действие цитокинов предопределяет развитие аутоиммунного или аллергического заболевания.
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