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Immunoglobulin and T Cell Antigen Receptor Gene Arrangements Indicate That the Immune Response in Autoimmune Thyroid Disease Is Polyclonal^*

WILHELM KAULFERSCH, JAMES R. BAKER, JR., KENNETH D. BURMAN, ANDREW J. AHMANN, JUAN C. D’AVIS and THOMAS A. WALDMANN

Metabolism Branch, National Cancer Institute, National Institutes of Health (W.K., T.A.W.) Bethesda, Maryland 20892
the Kyle Metabolic Unit and Transplant Immunology Service, Departments of Medicine and Surgery and Clinical Investigation, Walter Reed Army Medical Center (J.R.B., K.D.B., A.J.A., J.C.D.) Washington, D.C. 20307
the Department of Medicine, Uniformed Services University of Health Sciences Bethesda, Maryland 20814

Address requests for reprints to: Dr. Thomas A. Waldmann, Metabolism Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 4N115, Bethesda, Maryland 20892

To further define the degree of heterogeneity of the antibody and cellular immune responses in autoimmune thyroid disease, we used Southern blot hybridization techniques to analyze the arrangements of immunoglobulin and T cell antigen receptor genes in circulating lymphocytes and in those infiltrating the thyroid gland in nine patients with thyrotoxicosis due to Graves’ disease and five patients with Hashimoto’s thyroiditis. The sensitivity of these techniques was sufficient to detect a monoclonal population when there was as little as 1% clonal involvement in a mixed cell population.

In the patients studied, DNA from non-T peripheral blood cells and non-T intrathyroid lymphocytes had only a germline gene pattern and no clonal nongermline rearrangements of immunoglobulin genes, as assessed using an immunoglobulin joining heavy chain (IgJ_H) gene probe. An analysis of the DNA from peripheral blood T cells or intrathyroidal lymphocytes revealed polyclonal gene rearrangement patterns and no clonal nongermline rearrangements of the T cell antigen receptor-β and - genes, as assessed using T constant-β and T joining - gene probes.

These results indicate that the lymphocytes in peripheral blood and those infiltrating the thyroid gland in patients with autoimmune thyroid disease are of polyclonal origin.

^* The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Recipient of a Max Kade Foundation, Inc., stipend and of a Fogarty Visiting Fellowship.

Received June 30, 1987.