Skip to main content

Significance and Molecular Basis for IgG Glycosylation Changes in Rheumatoid Arthritis

  • Chapter
Book cover Glycoimmunology

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 376))

Abstract

Genetic and environmental factors are thought to contribute to either the initial susceptibility to synovitis or persistence of joint disease in patients with rheumatoid arthritis. The genetic component of the disease probably accounts for no more than 12–15% of the whole, only one-third to one-half of this component can be accounted for by genes encoded within the HLA complex which may influence disease severity rather than susceptibility (1). At present the recognition of specific HLA markers for more aggressive forms of the disease has not yet been translated into any form of successful therapy. Further, therapies aimed at CD4+ T-cells have not been successful, as also predicted from lack of amelioration of arthritis in AIDS patients. Clearly other risk factors need to be established in order for new therapeutic strategies to be developed.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Jawaheer, D., et al. 1994. Arthritis Rheum. 37:681–686.

    Article  PubMed  CAS  Google Scholar 

  2. Aho, K., et al. 1991. J. Rheumatol. 18:1282–1284.

    PubMed  CAS  Google Scholar 

  3. Tomana, M., et al. 1994. Rheumatol. Int. 13:217–220.

    Article  Google Scholar 

  4. Parekh, R.B., et al. 1988. J. Exp. Med. 167:1731–1736.

    Article  PubMed  CAS  Google Scholar 

  5. Parekh , R.B., et al. 1989. J. Autoimmun. 2:101–114.

    Article  PubMed  CAS  Google Scholar 

  6. Rademacher, T.W., 1991. Sem. Cell Biol. 2:327–337.

    CAS  Google Scholar 

  7. Rademacher, T.W., et al. 1988. Springer Semin. Immunopathol. 10:231–249.

    Article  PubMed  CAS  Google Scholar 

  8. Parekh, R.B., et al. 1985. Nature. 316:452–457.

    Article  PubMed  CAS  Google Scholar 

  9. Parekh, R.B. et al. 1988. Lancet. i:966–969.

    Article  Google Scholar 

  10. Dube, R., et al. 1990. Gut. 31:431–434.

    Article  PubMed  CAS  Google Scholar 

  11. Filley, E., et al. 1989. Clin. Exp. Immunol. 76:343–347.

    PubMed  CAS  Google Scholar 

  12. Rook, G.A.W. et al. 1991. Autoimmunity. 4:779–794.

    Article  CAS  Google Scholar 

  13. Young, A. et al. 1991. Arthritis Rheum. 34:1425–1429

    Article  PubMed  CAS  Google Scholar 

  14. Bodman, K. et al. 1994. Glycosylation & Disease. 1:219.

    Google Scholar 

  15. Van Zeben, D. et al. 1994. Br. J. Rheumatol. 33:36–43.

    Article  PubMed  Google Scholar 

  16. Van Zeben, D. 1993. J. Rheumatol. 20:1288–1296.

    PubMed  Google Scholar 

  17. Rademacher, et al. 1994. PNAS. 91:6123–6127.

    Article  PubMed  CAS  Google Scholar 

  18. Chang, C.Y. et al. 1994. J. Mol. Biol. 241:125–127.

    Article  PubMed  CAS  Google Scholar 

  19. Rademacher, T.W. 1994 in Animal Cell Biotechnology 6:5–22.

    CAS  Google Scholar 

  20. Malhotra R., et al. 1995. Nature. 1:237–243.

    Article  CAS  Google Scholar 

  21. Weinberg, J.B. et al. 1994. J. Exp. Med. 179:651–660.

    Article  PubMed  CAS  Google Scholar 

  22. McCartney-Francis, N., 1993. J.Exp. Med. 178:749–754.

    Article  PubMed  CAS  Google Scholar 

  23. Farrell, A.J., et al. 1992. Armal Rheum. Dis. 51:1219–1222.

    Article  CAS  Google Scholar 

  24. Kumpel, B.M., et al. 1994. Hum. Monoclonal Antibodies 5:143–151.

    CAS  Google Scholar 

  25. Wright, A., and Morrison, S.L. 1994. J.Exp. Med. 1087–1096.

    Google Scholar 

  26. Childs, R.A., 1990. J.Biol. Chem. 34:20770–20777.

    Google Scholar 

  27. Israel, E.J., et al. 1993. Immunol. 79:77–81.

    CAS  Google Scholar 

  28. Story, CM., et al. 1994. J.Exp. Med. 180:2377–2381.

    Article  PubMed  CAS  Google Scholar 

  29. Burmeister, W.P., et al. 1994. Nature. 372:379–383.

    Article  PubMed  CAS  Google Scholar 

  30. Burmeister, W.P. et al. 1994. Nature. 372:336–343.

    Article  PubMed  CAS  Google Scholar 

  31. Axford, J.S. et al. 1987. Lancet. 2:1486–1488.

    Article  PubMed  CAS  Google Scholar 

  32. Furukawa, K., et al. 1990 Int. Immunol. 2:105–112.

    Article  PubMed  CAS  Google Scholar 

  33. Wilson, I.B.H. 1993. J. Rheumatol. 20:1282–1287.

    PubMed  CAS  Google Scholar 

  34. Lund, J., et al. 1993. Molec. Immunol. 30:741–748.

    Article  CAS  Google Scholar 

  35. Field, M.C., et al. 1994. Biochem. J. 299:261–275.

    PubMed  CAS  Google Scholar 

  36. Sutherland, E.W. et al. 1972. PNAS 69:167–171.

    Article  PubMed  CAS  Google Scholar 

  37. Baumal, R. et al. 1971. J.Exp.Med. 134:1316–1334.

    Article  PubMed  CAS  Google Scholar 

  38. Hirano, T. et al. 1988. Eur. J. Immunol. 18:1797–1801.

    Article  PubMed  CAS  Google Scholar 

  39. Takai, Y., et al. 1989. Arthritis Rheum. 32:594–600.

    Article  PubMed  CAS  Google Scholar 

  40. Hitsumoto, Y., et al. 1992. Eur. J. Immunol. 1988:1797–1814.

    Google Scholar 

  41. Amara, J.F., et al. 1992. Trends in Cell Biol. 2:145–149.

    Article  CAS  Google Scholar 

  42. Randall, T.D., et al. 1992. PNAS. 89:962–966.

    Article  PubMed  CAS  Google Scholar 

  43. Hendershot, L.M., 1990. J.Cell. Biol. 111:829–837.

    Article  PubMed  CAS  Google Scholar 

  44. Knitter, M.R., & Hass, I.G., 1992. EMBO. 11:1573–1581.

    Google Scholar 

  45. Melnick, J., et al. 1992. J.Biol.Chem. 267:21303–21306.

    PubMed  CAS  Google Scholar 

  46. David, V, et al. 1993. J.Biol.Chem. 268:9585–9592.

    PubMed  CAS  Google Scholar 

  47. Galvin, K., et al. 1992. PNAS 89:8452–8456.

    Article  PubMed  CAS  Google Scholar 

  48. Hochstenbach, F., et al. 1992 PNAS 89:4734–4738.

    Article  PubMed  CAS  Google Scholar 

  49. Ou, W.-J., et al. 1993. Nature. 364:771–776.

    Article  PubMed  CAS  Google Scholar 

  50. Haffar, O.K. et al. 1988. J.Biol. Chem. 106:1463–1474.

    CAS  Google Scholar 

  51. Tarkowski, A., 1989. Arthritis Rheum. 32:1087–1092.

    Article  PubMed  CAS  Google Scholar 

  52. Bodman. K.B., et al. 1992. Clin. Exp. Immunol. 88:420–423.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1995 Springer Science+Business Media New York

About this chapter

Cite this chapter

Rademacher, T.W., Jones, R.H.V., Williams, P.J. (1995). Significance and Molecular Basis for IgG Glycosylation Changes in Rheumatoid Arthritis. In: Alavi, A., Axford, J.S. (eds) Glycoimmunology. Advances in Experimental Medicine and Biology, vol 376. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1885-3_20

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-1885-3_20

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5768-1

  • Online ISBN: 978-1-4615-1885-3

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics