Immunological studies of autoimmune thyroid disorders: abnormalities in the inducer T cell subset and proliferative responses to autologous and allogeneic stimulation

Various immunological parameters were investigated in patients with Hashimoto's thyroiditis (HT) and Graves' disease (GD). The total T cell numbers were significantly decreased in both diseases whether they were enumerated by E rosetting or by pan-T cell monoclonal antibodies (OKT3 and ant...

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Published inClinical and experimental immunology Vol. 54; no. 2; pp. 539 - 546
Main Authors FOURNIER, C, CHEN, H, LEGER, A, CHARREIRE, J
Format Journal Article
LanguageEnglish
Published Oxford Blackwell 01.11.1983
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Summary:Various immunological parameters were investigated in patients with Hashimoto's thyroiditis (HT) and Graves' disease (GD). The total T cell numbers were significantly decreased in both diseases whether they were enumerated by E rosetting or by pan-T cell monoclonal antibodies (OKT3 and anti-Leu 1). This diminution was due to a loss in the inducer T cell subset (OKT4+/Leu 3a+) whereas the cytotoxic/suppressor T cells (OKT8+/Leu 2a+) were present at normal levels in both diseases. The B cells were significantly higher in GD patients than in controls but were not modified in HT patients. Monocyte percentages remained unchanged and DR+ cells were slightly increased in the two diseases. On the other hand, T lymphocyte responses to stimulation by autologous or allogeneic cells were significantly impaired in GD but not in HT whether cultures were performed in autologous plasma or AB serum. In addition, lymphocytes from normal subjects were unable to proliferate in auto- or allo-MLR in the presence of plasma from GD patients but they were reactive in the presence of HT plasma or AB serum. Taken together, these results suggest that the patients with autoimmune thyroid disorders exhibit a T cell imbalance within the OKT4+/Leu 3a+ subset. Moreover, this abnormality is correlated with the observation that autoreactive and alloreactive cells are defective in GD.
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ISSN:0009-9104
1365-2249