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Evidence for Cell-Mediated Immunity and Specific Suppressor T Lymphocyte Dysfunction in Graves’ Disease and Diabetes Mellitus^*

DUNCAN TOPLISS, JACQUES HOW, MARK LEWIS, VAS ROW and ROBERT VOLPÉ

Department of Medicine, University of Toronto, and Endocrinology Research Laboratory, The Wellesley Hospital Toronto, Ontario, Canada

Address requests for reprints to: Dr. Robert Volpe, Department of Medicine, The Wellesley Hospital, 160 Wellesley Street East, Toronto, Ontario, M4Y 1J3 Canada.

Migration inhibition of purified peripheral T lymphocytes in response to pancreatic islet cell antigen or thyroid antigen was used to study cell-mediated immune mechanisms in patients with diabetes mellitus (IDDM) and Graves’ disease (GD). In response to islet cell antigen, T lymphocytes of subjects with IDDM for less than 3 yr exhibited migration inhibition, whereas those of normal subjects, noninsulin dependent diabetics, and subjects with IDDM for longer than 3 yr did not. Admixture of T lymphocytes from normal subjects with T lymphocytes from patients with IDDM for less than 3 yr substantially ameliorated the migration inhibition of the IDDM subjects to islet cell antigen. Migration of T lymphocytes from GD subjects was markedly inhibited by thyroid antigen and marginally inhibited by islet cell antigen. Admixture of GD T lymphocytes significantly ameliorated the migration inhibition of IDDM T lymphocytes to islet cell antigen, despite sensitization to thyroid antigen of the GD T lymphocytes.

We conclude: 1) sensitization to islet cell antigen in IDDM of recent onset is confirmed; 2) the ability of normal and GD T lymphocytes to ameliorate the migration inhibition of IDDM T lymphocytes strongly suggests correction of deficient suppressor T lymphocyte function; 3) the ability of GD T lymphocytes to ameliorate migration inhibition of IDDM T lymphocytes to islet cell antigen is evidence for an antigen-specific rather than a generalized suppressor T lymphocyte defect in GD; and 4) similarly, the normalization of migration index of GD T lymphocytes in response to thyroid antigen by those IDDM T lymphocytes not sensitized to thyroid antigen is again evidence for an antigen-specific and not a generalized suppressor T lymphocyte defect in IDDM.

^* This work was supported by a grant (MT859) from the Medical Research Council of Canada.

MRC (Canada) Research Fellow. Current Address: Endocrine Unit, Alfred Hospital, Melbourne, Australia 3181.

Fellow of the Wellesley Hospital Research Foundation.

Fellow of the Angus Foundation.

Received October 15, 1982.

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