Clinical and Experimental Pediatrics

The Korean Pediatric Society (대한소아청소년과학회)
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Autoimmunity

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  • Kim, Joong Gon (Department of Pediatrics, College of Medicine, Seoul National University)
  • 김중곤 (서울대학교 의과대학 소아과학교실)
  • Received : 2007.10.20
  • Accepted : 2007.11.25
  • Published : 2007.12.15
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Abstract

Self/non-self discrimination and unresponsiveness to self is the fundamental properties of the immune system. Self-tolerance is a state in which the individual is incapable of developing an immune response to an individual's own antigens and it underlies the ability to remain tolerant of individual's own tissue components. Several mechanisms have been postulated to explain the tolerant state. They can be broadly classified into two groups: central tolerance and peripheral tolerance. Several mechanisms exist, some of which are shared between T cells and B cells. In central tolerance, the recognition of self-antigen by lymphocytes in bone marrow or thymus during development is required, resulting in receptor editing (revision), clonal deletion, anergy or generation of regulatory T cells. Not all self-reactive B or T cells are centrally purged from the repertoire. Additional mechanisms of peripheral tolerance are required, such as anergy, suppression, deletion or clonal ignorance. Tolerance is antigen specific. Generating and maintaining the self-tolerance for T cells and B cells are complex. Failure of self-tolerance results in immune responses against self-antigens. Such reactions are called autoimmunity and may give rise to autoimmune diseases. Development of autoimmune disease is affected by properties of the genes of the individual and the environment, both infectious and non-infectious. The host's genes affect its susceptibility to autoimmunity and the environmental factors promote the activation of self-reactive lymphocytes, developing the autoimmunity. The changes in participating antigens (epitope spreading), cells, cytokines or other inflammatory mediators contribute to the progress from initial activation to a chronic state of autoimmune diseases.

Keywords

References

  1. Kindt TJ, Goldsby RA, Osborne BA. Kuby Immunology. 6th ed. New York: W.H.Freeman and Company, 2007:401- 24
  2. Kyewski B. Promiscuous gene expression and central T- cell tolerance: more than meets the eye. Trends Immunol 2002; 23:364-71 https://doi.org/10.1016/S1471-4906(02)02248-2
  3. Van Parijs L, Abbas AK: Homeostasis and self-tolerance in the immune system: turning lymphocytes off. Science 1998; 280:243-8 https://doi.org/10.1126/science.280.5361.243
  4. Conrad FJ, Rice JS, Cambier JC. Multiple paths to loss of anergy and gain autoimmunity. Autoimmunity 2007;40:418- 24 https://doi.org/10.1080/08916930701464723
  5. Ding C, Yan J. Regulation of autoreactive B cells: checkpoints and activation. Arch Immunol Ther Exp 2007;55:83- 9 https://doi.org/10.1007/s00005-007-0011-0
  6. Schwartz RH: T cell anergy. Ann Rev Immunol 2003;21:305- 34 https://doi.org/10.1146/annurev.immunol.21.120601.141110
  7. Walker LS, Abbas AK: The enemy within: keeping selfreactive T cells at bay in the periphery. Nat Rev Immunol 2002;2:11-9 https://doi.org/10.1038/nri701
  8. Viorritto ICB, Nikolov NP, Siegel RM. Autoimmunity versus tolerance: Can dying cells tip the balance. Clin Immunol 2007;122:125-34 https://doi.org/10.1016/j.clim.2006.07.012
  9. Mougneau E, Hugues S, Glaichenhaus N. Antigen presentation by dendritic cells in vivo. J Exp Med 2002;196:1013- 6 https://doi.org/10.1084/jem.20021636
  10. Gauld SB. Maintenance of B cell anergy requires constant antigen receptor occupancy and signalling. Nat Immunol 2005;6:1160-7 https://doi.org/10.1038/ni1256
  11. Steinman RM, Nussenzweig MC. Avoiding horror toxicus: the importance of dendritic cells in peripheral T cell tolerance. Proc Natl Acad Sci USA 2002;99:351-8
  12. Gattorno M, Martini A. The immune system and the inflammatory response. In: Cassidy JT, Petty RE, Laxer RM, Lindsley CB, editors. Textbook of Pediatric Rheumatology. 5th ed. Philadelphia: Elsevier Saunders, 2005:19-63
  13. Siegel RM, Chan FK, Chun HJ, Lenardo MJ. The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity. Nat Immunol 2000;1:469-74 https://doi.org/10.1038/82712
  14. Marrack P, Kappler J, Kotzin BL. Autoimmune disease;why and where it occurs. Nature Medicine 2001;7:899-905 https://doi.org/10.1038/90935
  15. Encinas JA, Kuchroo VK. Mapping and identification of autoimmunity genes. Curr Opin Immunol 2000;12:691-697 https://doi.org/10.1016/S0952-7915(00)00164-3
  16. Diamond B. Autoimmunity. Immunol Rev 2005;204:5-8 https://doi.org/10.1111/j.0105-2896.2005.00258.x
  17. Rioux JD, Abbas AK. Paths to undestanding the genetic basis of autoimmune disease. Nature 2005;435:584-9 https://doi.org/10.1038/nature03723
  18. Kukreja A, Maclaren NK. Autoimmunity and diabetes. J Clin Endocrinol Metab 1999;84:4371-8 https://doi.org/10.1210/jc.84.12.4371
  19. Ravetch JV, Bolland S. IgG receptors. Annu Rev Immunol 2001;19:275-90 https://doi.org/10.1146/annurev.immunol.19.1.275
  20. Criswell L. Familial clustering of disease features: Implications for the etiology and investigations of systemic autoimmune disease. Arthritis Rheum 2004;50:1707-8 https://doi.org/10.1002/art.20293
  21. Davidson A, Diamond B. Autoimmune diseases. N Engl J Med 2001;345:340-50 https://doi.org/10.1056/NEJM200108023450506
  22. Kim BS, Kaistha SD, Rouse BT. Viruses and autoimmunity. Autoimmunity 2006;39:71-7 https://doi.org/10.1080/08916930500484708
  23. O'Garra A, Steinman L, Gijbels K. CD4＋ T-cell subsets in autoimmunity. Curr Opin Immunol 1997;9:872-3 https://doi.org/10.1016/S0952-7915(97)80192-6
  24. Vanderlugt CL, Neville KL, Nikcevich KM, Eagar TN, Bluestone JA, Miller SD. Pathologic role and temporal appearance of newly emerging autoepitopes in relapsing experimental autoimmune encephalomyelitis. J Immunol 2000; 164:670-8 https://doi.org/10.4049/jimmunol.164.2.670
  25. Vanderlugt CL, Miller SD. Epitope spreading in immunemediated diseases: implications for immunotherapy. Nat Rev Immunol 2002;2:85-95 https://doi.org/10.1038/nri724
  26. Elkon K. Apoptosis and autoimmunity. In: Kalden JR, Herrmann M, editors. From Mechanisms to Treatments. Weinheim: Wiley-VCH verlag Gmbh & Co, 2003:3-11
  27. Manfredi AA, Rovere P, Galati G, Heltai S, Bozzolo E, Soldini L, et al. Apoptotic cell clearance in systemic lupus erythematosus: I. Opsonization by antiphospholipid antibodies. Arthritis Rheum 2004;41:205-14 https://doi.org/10.1002/1529-0131(199802)41:2<205::AID-ART4>3.0.CO;2-0
  28. McCartney-Francis NL, Frazier-Jessen M, Wahl SM, TGF-beta: a balancing act. Int Rev Immunol 1998;16:553-80 https://doi.org/10.3109/08830189809043009
  29. Stassi G, Di Liberto D, Todaro M, Zeuner A, Ricci-Vitiani L, Stoppacciaro A, et al. Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins. Nat Immunol 2000;1:483-8 https://doi.org/10.1038/82725

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