medigraphic.com
ISSN 1817-5996 (Digital)

2012, Número 19

<< Anterior Siguiente >>

Rev Cub de Reu 2012; 14 (19)


Mecanismos inmunológicos y blanco de las lesiones inflamatorias

Suárez MR, Remedios BSE, Serrano EI

Idioma: Español
Referencias bibliográficas: 70
Paginas:
Archivo PDF: 124.54 Kb.


RESUMEN

En la Espondilitis Anquilopoyética al igual que en resto de las enfermedades que corresponden al grupo de las espondiloartritis, su etiopatogenia no está bien establecida; en ella intervienen muchos factores como son la asociación genética, herencia y respuesta inflamatoria, así como su relación con infecciones endógenas, comportándose de manera distinta a otras enfermedades reumáticas inflamatorias. Se realiza una revisión bibliográfica del proceso inflamatorio que se desarrolla en la Espondilitis Anquilosante como parte significativa en la etiopatogenia de la enfermedad, recuperando 118 citas bibliográficas de las revistas de mayor impacto dentro de la especialidad de reumatología, a las que se pudo acceder a través de Hinari, Pud Med, Bireme, SciELO, Ebsco y Perii, excluyendo 48 que no se ofrecían con acceso abierto o no fueron útiles para el objetivo de nuestra revisión, quedándonos con 70 artículos a texto completo que nos ofrecían los datos necesario para actualizar el tema que nos propusimos revisar.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Sieper J, Braum J, Rutwaleit M, Boone A, Zink A. Ankylosing Spndylitis: an overview. Ann. Rheum. Diss. 2001; 61.

  2. Vergara M P. Patogenia de las Artropatías Seronegativas. Rev. Chil. Reumatol. 2009; 25(2):88-99.

  3. McGonagle D, Gibbon W, Emery P: Classification of inflammatory arthritis by enthesitis. Lancet. 1998; 352:1137- 40.

  4. Broun J, Khan M.A, Sierper J. Enthesitis and ankylosing in spondyloarthropathy: What is the target of thwe inmune response? Ann. Rheum. Diss. 2000; 59: 985- 94.

  5. Benjamin M, McGonagle D: The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites. J Anat. 2001; 199:503- 26.

  6. Benjamin M, Moriggl B, Brenner E, Emery P, McGonagle D, Redman S: The 'enthesis organ' concept: why enthesopathiesmay not present as focal insertional disorders. Arthritis Rheum. 2004; 50:3306- 13.

  7. McGonagle D, Lories RJ, Tan A, Benjamin M: The concept of a synovio-entheseal complex and its implications for understanding joint inflammation and damage in psoriatic arthritis and beyond. Arthritis Rheum. 2007; 56:2482- 91.

  8. Melis L; Elewant D. Progress in spondyloarthritis. Inmunopatogenesis of spondyloarthritis: Which cells drive disease. Arthritis Research &Therapy. 2009; 11: 233- 37.

  9. Breban M: Genetics of spondyloarthritis. Best Pract Res Clin Rheumatol. 2006, 20: 593- 99.

  10. Francois RJ, Gardner DL, Degrave EJ, Bywaters EG: Histopathologic evidence that sacroiliitis in ankylosing spondylitis is not merely enthesitis. Arthritis Rheum. 2000; 43: 2011- 24.

  11. Schett G: Joint remodelling in inflammatory disease. Ann Rheum Dis. 2007, 66 (Suppl 3): 42- 4.

  12. Van Echteld I, Cieza A, Boonen A, et al. Identification of the most common problemsby patients with ankylosing spondylitis using the internationalclassification of functioning, disability and health. J Rheumatol. 2006; 33:2475- 83

  13. Cañete JD, Rodríguez JR, Salvador GS, Gómez A, Muñoz J, Sanmartí R. Diagnostic usefulness of sinovial vascular morphology in chronic arthritis. A systematic survey of 100 cases. Semin Arthritis Rheum. 2003; 32: 378-87.

  14. Baeten D, Demetter P, Cuvelier C, et al. Comparative study of synovial histology in rheumatoid arthritis, spondyloarthropathy and osteoarthritis: influence of disease duration and activity. Ann Rheum Dis. 2000; 59: 945-53.

  15. Leong TT, Fearon U, Veale DJ. Angiogenesis in psoriasis and psoriatic arthritis: clues to disease pathogenesis. Curr Rheumatol Rep. 2005; 7: 325-9.

  16. Cañete JD, Pablos JL, Sanmartí R, Mallofré C, Marsal S, Maymó J, et al. Antiangiogenic effects of anti-tumor necrosis factor alpha therapy with infliximab in psoriatic arthritis. Arthritis Reum. 2004; 50: 1636- 41.

  17. Hou TY, Chen HC, Chen CH, Chang DM, Liu FC, Lai JH. Usefulness of human leucocyte antigen-B27 subtypes in predicting ankylosing spondylitis: Taiwan experience. Intern Med J. 2007; 37:749-52.

  18. D'Amato M, Fiorillo MT, Carcassi C, et al. Relevance of residue 116 of HLAB27 in determining susceptibility to ankylosing spondylitis. Eur J Immunol. 1995; 25: 3199-201.

  19. Maksymowych WP, Rahman P, Reeve JP, et al. Association of the IL1 gene cluster with susceptibility to ankylosing spondylitis: an analysis of three Canadian populations. Arthritis Rheum. 2006; 54: 974-85.

  20. Van der Heigd D, Maksymowych W P. et al. Spondyloarthritis: state of the art and future perspectives. Ann. Rheumt Diss. 2010; 69: 949- 54.

  21. Baeten D, Moller HJ, Delanghe J, Veys EM, Moestrup SK, De Keyser F: Association of CD163+ macrophages and local production of soluble CD163 with decreased lymphocyte activation in spondylarthropathy synovitis. Arthritis Rheum. 2004; 50:1611- 23.

  22. McGonagle D, Marzo-Ortega H, O'Connor P, Gibbon W, Hawkey P, Henshaw K, Emery P: Histological assessment of the early enthesitis lesion in spondyloarthropathy. Ann Rheum Dis. 2002; 61: 534- 37.

  23. De Rycke L, Kruithof E, Vandooren B,Tak PP, Baeten D. Pathogenesis of spondyloarthritis: insights from synovial membrane studies. Curr Rheum Rep. 2006; 8: 275-82.

  24. Baeten D, Demetter P, Cuvelier CA, et al. Macrophages expressing the scavenger receptor CD163: a link between immune alterations of the gut and synovial inflammation in spondyloarthropathy. J Pathol. 2002; 196: 343-50.

  25. Kruithof E, De Rycke L, Vandooren B, et al. Identification of synovial biomarkers of response to experimental treatmentin early phase clinical trials in spondylarthropathy. Arthritis Rheum. 2006; 54: 1795-804.

  26. Cañete JD, Santiago B, Canta T, et al Ectopic lymphoid neogenesis in psoriatic arthritis. Ann Rheum Dis. 2007; 66:720.

  27. Iwahashi M, Yamamura M, Aita T, et al. Expression of Toll-like receptor 2 on CD16+ blood monocytes and synovial tissue macrophages in rheumatoid arthritis. Arthritis Rheum. 2004; 50: 1457- 67.

  28. De Rycke L, Vandooren B, Kruithof E, et al. Tumor necrosis factor alpha blockade treatment down-modulates the increased systemic and local expression of Toll-like receptor 2 and Toll-like receptor 4 in spondylarthropathy. Arthritis Rheum. 2005; 52: 2146- 58.

  29. Candia L, Marquez J, Hernández C, Zea AH, Espinoza LR. Toll-like receptor-2 expression is upregulated in antigen-presenting cells from patients with psoriatic arthritis: a pathogenic role for innate immunity? J Rheumatol. 2007; 34: 374- 9.

  30. Kruithof E, Baeten D, De Rycke L, et al. Synovial histopathology of psoriatic arthritis, both oligo- and polyarticular, resembles spondyloarthropathy more than it does rheumatoid arthritis. Arthritis Res Ther. 2005; 7: 569- 80.

  31. Rudwaleit M, Siegert S, Yin Z, et al. Low T cell production of TNFalpha and IFNgamma in ankylosing spondylitis: its relation to HLA-B27 and influence of the TNF-308 gene polymorphism. Ann Rheum Dis. 2001; 60: 36-42.

  32. Beaten D, et al. Impaired Th1 cytokine production in spondyloarthropaty is restored by anti-TNF alpha. Ann. Rheum. Dis. 2001; 60: 750- 55.

  33. Cuvelier C, Barbatis C, Mielants H, De Vos M, Roels H, Veys E: Histopathology of intestinal inflammation related to reactive arthritis. Gut. 1987; 28:394- 01.

  34. Szekanecz Z, Koch AE: Mechanisms of disease: angiogenesis in inflammatory diseases. Nat Clin Pract Rheumatol 2007, 3:635-643.

  35. Tam, LS, Gu, J, David Y.Pathogenesis of ankylosing spondylitis. Nat. Rev. Rheumatol.2010; 6: 399- 405.

  36. Laloux L, Voisin MC, Allain J, et al. Immunohistological study of entheses in spondyloarthropathies: comparison in rheumatoid arthritis and osteoarthritis. Ann Rheum Dis. 2001; 60: 316- 21.

  37. Appel H, Kuhne M, Spiekermann S, et al. Immunohistologic analysis of zygapophyseal joints in patients with ankylosing spondylitis. Arthritis Rheum. 2006; 54: 2845- 51.

  38. Baraliakos X, Listing J, Rudwaleit M, Sieper J, Braun J. The relationship between inflammation and new bone formation in patients with ankylosing spondylitis. Arthritis Research & Therapy. 2008; 10: 104.

  39. Braun J, Bollow M, Neure L, Seipelt E, Seyrekbasan F, Herbst H, Eggens U, Distler A, Sieper J: Use of immunohistologic and in situ hybridization techniques in the examination of sacroiliacjoint biopsy specimens from patients with ankylosingspondylitis. Arthritis & Rheum. 1995; 38: 499- 505.

  40. François RJ, Neure L, Sieper J, Braun J: Immunohistological examination of open sacroiliac biopsies of patients with ankylosing spondylitis: detection of tumour necrosis factor {alpha} in two patients with early disease and transforming growth factor {beta} in three more advanced cases. Ann Rheum Dis. 2006; 65:713- 20.

  41. Duchmann R, Lambert C, May E, Hahler T, Marker-Hermann E. CD-4+ and CD-8+ clonal T cell expansions indicate a role of antigens in ankylosing spondylitis: a study in HLA-B27+ monozygotics twins. Clin. Exp. Inmunol. 2001; 123 (2): 314- 22.

  42. Beaten D, et al. Impaired Th1 cytokine production in spondyloarthropaty is restored by anti-TNF alpha. Ann. Rheum. Dis. 2001; 60: 750- 55.

  43. Lories RJ, Derese I, Luyten FP: Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis. J Clin Invest. 2005; 115:1571- 79.

  44. Sieper J, Braum J, Rutwaleit M, Boone A, Zink A. Ankylosing Spndylitis: an overview. Ann. Rheum. Diss. 2001: 61.

  45. Tourog J. D. HLA-DR4 and spondyloarthropaties. Ann. Rheum. Diss. 2002; 61: 193- 94.

  46. Firestein GS. Evolving concepts of rheumatoid arthritis. Nature. 2003; 423 (6937): 356- 61.

  47. Layh-Schmitt, G, Colbert, R. A. The interleukin-23/interleukin-17 axis in spondyloarthritis. Curr. Opin. Rheumatol. 2008; 20: 392- 97.

  48. Turner, M. J., Delay, M. L., Bai, S., Klenk, Colbert, R. A. HLA-B27 up-regulation causes accumulation of misfolded heavy chains and correlates with the magnitude of the unfolded protein response in transgenic rats: implications for the pathogenesis of spondylarthritis-like disease. Arthritis Rheum. 2007; 56: 215-223.

  49. Colbert, R. A., DeLay, M. L., Layh-Schmitt, G. Sowders, D. P. HLA-B27 misfolding and spondyloarthropathies. Prion. 2009; 3, 15- 26.

  50. Smith, J. A. et al. endoplasmic reticulum stress and the unfolded protein response are linked to synergistic iFN-beta induction via X-box binding protein 1. Eur. J. Immunol. 2008; 38: 1194- 203.

  51. Basso AS, Cheroutre H, et al. More stories on Th17 cells. Cell Res. 2009; 19 (4): 399-411.

  52. Wellcome Trust Case Control Consortium; Australo-Anglo-American Spondylitis Consortium (TASC), Burton PR, Clayton DG, Cardon LR, Craddock N, Deloukas P, Duncanson A, et al.: Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. Nat Genet. 2007; 39:1329- 37.

  53. Rueda B, Orozco G, Raya E, Fernandez-Sueiro JL, Mulero J, Blanco FJ, Vilches C, Gonzalez-Gay MA, Martin J: The IL23R Arg381Gln non-synonymous polymorphism confers susceptibility to ankylosing spondylitis. Ann Rheum Dis. 2008; 67:1451- 54.

  54. Kastelein RA, Hunter CA, Cua DJ. Discovery and biology of IL-23 and IL-27: related but functionally distinct regulators of inflammation. Annu Rev Immunol. 2009; 25: 221- 42

  55. Langrish CL, Chen Yet al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med 2005; 201(2): 233-240

  56. Ivanov II, Zhou L, Littman DR. Transcriptional regulation of Th17 cell differentiation. Semin Immunol. 2007; 19 (6): 409- 17.

  57. Turner, M. J., Delay, M. L., Bai, S., Klenk, Colbert, R. A. HLA-B27 up-regulation causes accumulation of misfolded heavy chains and correlates with the magnitude of the unfolded protein response in transgenic rats: implications for the pathogenesis of spondylarthritis-like disease. Arthritis Rheum. 2007; 56: 215-223.

  58. Colbert, R. A., DeLay, M. L., Layh-Schmitt, G. Sowders, D. P. HLA-B27 misfolding and spondyloarthropathies. Prion. 2009; 3: 15-26.

  59. Smith, J. A. et al. endoplasmic reticulum stress and the unfolded protein response are linked to synergistic iFN-beta induction via X-box binding protein 1. Eur. J. Immunol. 2008; 38: 1194- 203.

  60. Shen H, Goodall JC et al. Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis. Arthritis Rheum. 2009; 60 (6): 1647- 56.

  61. Wang X, Lin Z, Wei Q. et al. Expression of IL-23 and IL-17 and effect of IL-23 on IL-17 production in ankylosing spondylitis. Rheumatol Int. 2009; 29 (11): 1343- 47.

  62. Cañete Crespillo JD. Inflamación en las espondiloartritis: aspectos diferenciales. Reumatol Clin. 2007;3 (Supl 2): 19-23.

  63. Mei Y, Pan F, Gao J, Ge R, Duan Z, Zeng Z, et al. Increased serum IL-17 and IL-23 in the patient with ankylosing spondylitis. Clin Rheumatol. 2011; 30:269- 73.

  64. Harrington LE, Hatton RD et al. Interleukin 17- producing CD4 effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat Immunol 2005; 6 (11):1123- 32.

  65. Murphy CA, Langrish CL et al. Divergent pro- and antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J Exp Med. 2003; 198 (12): 1951- 57

  66. Becker C, Dornhoff H et al. Cutting edge: IL-23 crossregulates IL-12 production in T cell-dependent experimental colitis. J Immunol 2006; 177 (5): 2760-2764.

  67. Bettelli E, Oukka M, Kuchroo VK. Th-17 cells in the circle of immunity and autoimmunity. Nat Immunol. 2007; 8 (4): 345- 50.

  68. Jandus C, Bioley G, Rivals JP, Dudler J, Speiser D, Romero P. Increased numbers of circulating polyfunctional Th17 memory cells in patients with seronegative spondylarthritides. Arthritis & Rheum. 2008; 58:2307- 17.

  69. Singh R, Aggarwal A, Misra R: Th1/Th17 cytokine profiles in patients with reactive arthritis/undifferentiated spondyloarthropathy. J Rheumatol. 2007; 34: 2285- 90.

  70. Baeten D, Kruithof E, Breban M, Tak P. Spondylarthritis in the absence of B lymphocytes. Arthritis Rheum. 2008; 58: 730- 33.




2020     |     www.medigraphic.com