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Nontoxic Nodular Goiter and Papillary Thyroid Carcinoma Are Not Associated With Peripheral Blood Lymphocyte Sensitization to Thyroid Cells^*

JAIME AGUAYO, YOSHIKI SAKATSUME, CHRISTOPHER JAMIESON, VAS V. ROW and ROBERT VOLPÉ

Endocrinology Research Laboratory, Wellesley Hospital, University of Toronto Toronto, Ontario, Canada

Address all correspondence and requests for reprints to: Dr. Robert Volpe, Endocrinology Research Laboratory, Wellesley Hospital, University of Toronto, 160 Wellesley Street E, Room 112D Jones Bldg., Toronto, Ontario, M4Y1J3 Canada.

We tested the claim that uni- and multinodular goiter (UNG and MNG) and papillary carcinoma (PC) of the thyroid are autoimmune thyroid diseases (AITD) similar to Graves' disease (GD) and Hashimoto's thyroiditis (HT). The expression of HLA-DR on cultured thyroid epithelial cells (thyrocytes) from UNG, MNG, and PC after coculture with autologous peripheral blood mononuclear cells (PBMC) was compared with that on GD and HT cells. The thyrocytes also were cultured with interferon- (IFN) alone. A cytotoxicity assay involving ⁵¹Cr-labeled thyrocytes, anti-HLA-DR, and complement was used to determine HLA-DR expression. Stimulation of thyrocytes with 200 U/mL IFN induced HLA-DR (expressed as a cytotoxicity index) equally well on all thyrocytes [AITD (n = 6): IFN7, 23.8 ± 7.7 (±SD); unstimulated, 3.6 ± 2.0; UNG (n = 6), MNG (n = 9), and PC (n = 5): IFN7, 22.5 ± 4.7;unstimulated, 4.0 ± 3.0]. When cocultured with autologous PBMC, the values were: AITD, 24.9 ± 10.1; UNG, MNG, and PC, 3.8 ± 3.7 (P < 0.001). The supernatants from the AITD cocultures had higher IFN concentrations (by RIA) than those from the other cocultures.

We conclude that in UNG, MNG, and PC, the peripheral blood helper T-lymphocytes are not sensitized to thyrocyte membrane antigen(s); consequently, little if any IFN is producedin cocultures, and hence, there is no increase in thyrocyte HLA-DR expression, unlike the situation in AITD (GD and HT). Thus, UNG, MNG, and PC are not primarily autoimmune in nature, as defined by a lack of sensitization of the PBMC of such patients to thyroid antigen(s).

^* This work was supported by a grant (MT850) from the Medical Research Council of Canada. Parts of this study were presented at the International Congress of Endocrinology, July 14–17, 1988, Kyoto, Japan.

Fellow of the Angus Foundation, Wellesley Hospital, Toronto, Ontario, Canada.

Received June 3, 1988.

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