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. 1985 Feb;59(2):377–382.

Activated T cells in Graves' disease before treatment.

R Kennedy, U Di Mario, P Pozzilli, K Guy, M Leonardi, M Sensi, D Andreani
PMCID: PMC1577135  PMID: 3156702

Abstract

The aim of this study was the definition of abnormalities occurring within T-cell subsets of thyrotoxic Graves' patients before treatment. Special emphasis was placed on the enumeration of activated T cells using a number of new monoclonal antibodies. Lymphocytes from 22 Graves' disease patients were examined. The total number, the percentage of 'helper/inducer' and 'suppressor/cytotoxic' positive cells were evaluated using the antibodies T3, T4 and UCHT4, whereas the cells with killer activity were defined by H25. Activated T cells were detected using the antibodies DA6.231, DA6.164, and L243 which bind different epitopes of the beta chains of class II surface antigens and 4F2, which binds a 120,000 molecular weight glycoprotein. The results show no significant change in the total T, helper or suppressor cell phenotype, but an increase in the killer cell percentage was noted. Of those patients tested, 19 of 22 showed an increase in activated T cells, 18 of 22 patients showed a significant increase of T cells bearing class II antigens, 11 of 22 showed an increase of T cells staining with another activated T cell antibody, 4F2. The anti-DR antibodies expressed different binding characteristics, the most striking difference being seen between the antibodies DA6.231 and L243. The results of this study suggest an heterogeneity of the immune response, or differences in activation stage in patients with Graves' disease before therapeutic intervention. An important role for these cells in the pathogenesis of this disorder can be inferred.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bai Y., Beverley P. C., Knowles R. W., Bodmer W. F. Two monoclonal antibodies identifying a subset of human peripheral mononuclear cells with natural killer cell activity. Eur J Immunol. 1983 Jul;13(7):521–527. doi: 10.1002/eji.1830130702. [DOI] [PubMed] [Google Scholar]
  2. Bottazzo G. F., Pujol-Borrell R., Hanafusa T., Feldmann M. Role of aberrant HLA-DR expression and antigen presentation in induction of endocrine autoimmunity. Lancet. 1983 Nov 12;2(8359):1115–1119. doi: 10.1016/s0140-6736(83)90629-3. [DOI] [PubMed] [Google Scholar]
  3. Calder E. A., Irvine W. J., Davidson N. M., Wu F. T, B and K cells in autoimmune thyroid disease. Clin Exp Immunol. 1976 Jul;25(1):17–22. [PMC free article] [PubMed] [Google Scholar]
  4. Di Mario U., Guy K. Evaluation of class II antigen positive T cells: a simple double staining method using monoclonal antibodies. J Clin Lab Immunol. 1984 Apr;13(4):203–204. [PubMed] [Google Scholar]
  5. Eisenbarth G. S., Haynes B. F., Schroer J. A., Fauci A. S. Production of monoclonal antibodies reacting with peripheral blood mononuclear cell surface differentiation antigens. J Immunol. 1980 Mar;124(3):1237–1244. [PubMed] [Google Scholar]
  6. Gonwa T. A., Picker L. J., Raff H. V., Goyert S. M., Silver J., Stobo J. D. Antigen-presenting capabilities of human monocytes correlates with their expression of HLA-DS, an Ia determinant distinct from HLA-DR. J Immunol. 1983 Feb;130(2):706–711. [PubMed] [Google Scholar]
  7. Guy K., Van Heyningen V., Cohen B. B., Deane D. L., Steel C. M. Differential expression and serologically distinct subpopulations of human Ia antigens detected with monoclonal antibodies to Ia alpha and beta chains. Eur J Immunol. 1982 Nov;12(11):942–948. doi: 10.1002/eji.1830121109. [DOI] [PubMed] [Google Scholar]
  8. Hurley C. K., Nunez G., Winchester R., Finn O. J., Levy R., Capra J. D. The human HLA-DR antigens are encoded by multiple beta-chain loci. J Immunol. 1982 Nov;129(5):2103–2108. [PubMed] [Google Scholar]
  9. Jackson R. A., Haynes B. F., Burch W. M., Shimizu K., Bowring M. A., Eisenbarth G. S. Ia+ T cells in new onset Graves' disease. J Clin Endocrinol Metab. 1984 Aug;59(2):187–190. doi: 10.1210/jcem-59-2-187. [DOI] [PubMed] [Google Scholar]
  10. Kratzin H., Yang C. Y., Götz H., Pauly E., Kölbel S., Egert G., Thinnes F. P., Wernet P., Altevogt P., Hilschmann N. Primärstruktur menschlicher Histokompatibilitätsantigene der Klasse II. 1. Mitteilung: Aminosäuresequenz der N-terminalen 198 Reste der beta-Kette des HLA-Dw2,2;DR2,2-Alloantigens. Hoppe Seylers Z Physiol Chem. 1981 Dec;362(12):1665–1669. [PubMed] [Google Scholar]
  11. Lampson L. A., Levy R. Two populations of Ia-like molecules on a human B cell line. J Immunol. 1980 Jul;125(1):293–299. [PubMed] [Google Scholar]
  12. Ludgate M. E., McGregor A. M., Weetman A. P., Ratanachaiyavong S., Lazarus J. H., Hall R., Middleton G. W. Analysis of T cell subsets in Graves' disease: alterations associated with carbimazole. Br Med J (Clin Res Ed) 1984 Feb 18;288(6416):526–530. doi: 10.1136/bmj.288.6416.526. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Pozzilli P., Andreani D. Increased 'killer' cells in Graves' disease. Horm Metab Res. 1982 Jan;14(1):56–56. doi: 10.1055/s-2007-1018922. [DOI] [PubMed] [Google Scholar]
  14. Pujol-Borrell R., Hanafusa T., Chiovato L., Bottazzo G. F. Lectin-induced expression of DR antigen on human cultured follicular thyroid cells. Nature. 1983 Jul 7;304(5921):71–73. doi: 10.1038/304071a0. [DOI] [PubMed] [Google Scholar]
  15. Sensi M., Pozzilli P., Di Mario U. A method to facilitate the reading of up to 60 samples of monoclonal antibody-fluorescence stained cells using Medicell HLA-DR plates. J Clin Lab Immunol. 1984 Feb;13(2):101–102. [PubMed] [Google Scholar]
  16. Sridama V., Pacini F., DeGroot L. J. Decreased suppressor T-lymphocytes in autoimmune thyroid diseases detected by monoclonal antibodies. J Clin Endocrinol Metab. 1982 Feb;54(2):316–319. doi: 10.1210/jcem-54-2-316. [DOI] [PubMed] [Google Scholar]
  17. Strakosch C. R., Wenzel B. E., Row V. V., Volpé R. Immunology of autoimmune thyroid diseases. N Engl J Med. 1982 Dec 9;307(24):1499–1507. doi: 10.1056/NEJM198212093072407. [DOI] [PubMed] [Google Scholar]
  18. Thielemans C., Vanhaelst L., de Waele M., Jonckheer M., Van Camp B. Autoimmune thyroiditis: a condition related to a decrease in T-suppressor cells. Clin Endocrinol (Oxf) 1981 Sep;15(3):259–263. doi: 10.1111/j.1365-2265.1981.tb00664.x. [DOI] [PubMed] [Google Scholar]
  19. Volpé R. The pathogenesis of Graves' disease: an overview. Clin Endocrinol Metab. 1978 Mar;7(1):3–29. doi: 10.1016/s0300-595x(78)80033-4. [DOI] [PubMed] [Google Scholar]
  20. Wall J. R., Baur R., Schleusener H., Bandy-Dafoe P. Peripheral blood and intrathyroidal mononuclear cell populations in patients with autoimmune thyroid disorders enumerated using monoclonal antibodies. J Clin Endocrinol Metab. 1983 Jan;56(1):164–169. doi: 10.1210/jcem-56-1-164. [DOI] [PubMed] [Google Scholar]
  21. Winchester R. J., Kunkel H. G. The human Ia system. Adv Immunol. 1979;28:221–292. [PubMed] [Google Scholar]
  22. van Heyningen V., Guy K., Newman R., Steel C. M. Human MHC class II molecules as differentiation markers. Immunogenetics. 1982;16(5):459–469. doi: 10.1007/BF00372104. [DOI] [PubMed] [Google Scholar]

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