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The Effect of Cyclosporin a on Spontaneous Autoimmune Thyroiditis in Obese Strain (OS) Chickens

  • Georg Wick
  • Richard L. Boyd
  • Pia U. Muller
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 149)

Abstract

For the last twelve years data were accumulated by several groups that spontaneous autoimmune thyroiditis (SAT) which develops in the Obese strain (OS) of chickens depends on the presence of an intact B-dependent portion of the immune system (for review see refs. 1,2). Four types of effector mechanisms can be conceived as initiators of this disease and have been studied in detail: (a) complement binding thyroglobulin autoantibodies (Tg-AAb) either transferred from the mother hen via the egg yolk into the embryo and newly hatched chick or produced by the chick itself; (b) noncomplement binding IgG Tg-AAb triggering antibody-dependent cellular cytotoxicity (ADCC) by K-cells; (c) the occurrence of B-cells or mature plasma cells within the thyroid epithelial cell lining, a process called “periopolesis,” where formation of Tg-AAb has been demonstrated in situ which can again either bind complement or not and lead to a destruction or neighboring thyroid epithelial cells by mechanisms (a) or (b); (d) cytotoxic T-cells (Tc).

Keywords

Autoimmune Thyroiditis Skin Allograft Skin Graft Survival Obese Strain Skin Allograft Survival 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    G. Wick, R.S. Sundick, and B. Albini. Clin. Immunol. Immunopathol. 3:272 (1974).PubMedCrossRefGoogle Scholar
  2. 2.
    G. Wick, R. Boyd, K. Hala, L. de Carvalho, R. Kofler, P. Muller, and R.K. Cole. Curr. Top Microbiol. Immunol. 91:109 (1981).PubMedCrossRefGoogle Scholar
  3. 3.
    R. Boyd, and G. Wick, in: “Autoimmune Aspects of Endocrine Disorders,” A. Pinchera, D. Doniach, G.F. Fenzi, and L. Baschieri, eds., Academic Press, London-N.Y., p. 199 (1980).Google Scholar
  4. 4.
    L.C. Pontes de Carvalho, G. Wick, and I.M. Roitt. J. Immunol. 126:750 (1981).Google Scholar
  5. 5.
    J.F. Borel, C. Feurer, H.U. Gubler, and H. Stahelin. Eur. J. Immunol., in press (1981).Google Scholar
  6. 6.
    D. Bunjes, C. Hardt, M. Rollinghoff, and H. Wagner, Eur. J. Immunol, in press (1981).Google Scholar
  7. 7.
    A. Kunkl, G.G.B. Klaus. J. Immunol. 125:2526 (1980).PubMedGoogle Scholar
  8. 8.
    G. Wick, P.U. Muller, R. Boyd, and S. Schwarz, in preparation.Google Scholar
  9. 9.
    C.I. Green, A.C. Allison, and S. Precious. Lancet ii, 123 (1979).CrossRefGoogle Scholar
  10. 10.
    R.Y. Calne. Immunol. Rev. 46:113 (1979).PubMedCrossRefGoogle Scholar
  11. 11.
    J.F. Bone. Transpl. Proc. 13:344 (1981).Google Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • Georg Wick
    • 1
  • Richard L. Boyd
    • 1
  • Pia U. Muller
    • 1
  1. 1.Institute for General and Experimental Pathology, Medical SchoolUniversity of InnsbruckInnsbruckAustria

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