Human T Cell Leukemia Virus Type I-Infected Patients with Hashimoto’s Thyroiditis and Graves’ Disease

Context: Autoimmune thyroid diseases have been reported to be associated with human T cell leukemia virus type I (HTLV-I) infection. HTLV-I proviral load is related to the development of HTLV-I-associated myelopathy/tropical spastic paraparesis and has also been shown to be elevated in the periphera...

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Published inThe journal of clinical endocrinology and metabolism Vol. 90; no. 10; pp. 5704 - 5710
Main Authors Matsuda, Takehiro, Tomita, Mariko, Uchihara, Jun-Nosuke, Okudaira, Taeko, Ohshiro, Kazuiku, Tomoyose, Takeaki, Ikema, Tomoki, Masuda, Masato, Saito, Mineki, Osame, Mitsuhiro, Takasu, Nobuyuki, Ohta, Takao, Mori, Naoki
Format Journal Article
LanguageEnglish
Published Bethesda, MD Endocrine Society 01.10.2005
Copyright by The Endocrine Society
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Summary:Context: Autoimmune thyroid diseases have been reported to be associated with human T cell leukemia virus type I (HTLV-I) infection. HTLV-I proviral load is related to the development of HTLV-I-associated myelopathy/tropical spastic paraparesis and has also been shown to be elevated in the peripheral blood of HTLV-I-infected patients with uveitis, arthritis, and connective tissue disease. Objective: The objective of the study was to evaluate the proviral load in HTLV-I-infected patients with Hashimoto’s thyroiditis (HT) or Graves’ disease (GD) and ascertain the ability of HTLV-I to infect thyroid cells. Patients and Methods: A quantitative real-time PCR assay was developed to measure the proviral load of HTLV-I in peripheral blood mononuclear cells from 26 HTLV-I-infected patients with HT, eight HTLV-I-infected patients with GD, or 38 asymptomatic HTLV-I carriers. Rat FRTL-5 thyroid cells were cocultured with HTLV-I-infected T cell line MT-2 or uninfected T cell line CCRF-CEM. After coculture with T cell lines, changes in Tax and cytokine mRNA expression were studied by RT-PCR. Results: HTLV-I proviral load was significantly higher in the peripheral blood of patients with HT and GD than asymptomatic HTLV-I carriers. In the peripheral blood from HTLV-I-infected patients with HT, HTLV-I proviral load did not correlate with the thyroid peroxidase antibody or thyroglobulin antibody titer. After coculture with MT-2 cells, FRTL-5 cells expressed HTLV-I-specific Tax mRNA. These cocultured FRTL-5 cells with MT-2 cells expressed IL-6 mRNA and proliferated more actively than those cocultured with CCRF-CEM cells. Conclusion: Our findings suggest the role of the retrovirus in the development of autoimmune thyroid diseases in HTLV-I-infected patients.
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ISSN:0021-972X
1945-7197
DOI:10.1210/jc.2005-0679