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Primary T-cell lymphoma of the thyroid gland with chemokine receptors of Th1 phenotype complicating autoimmune thyroiditis

Department of Hematology, Molecular Medicine Unit, Atomic Bomb Disease Institute, and Department of Laboratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Department of Pathology, School of Medicine, Kurume University, Kurume, Japan, Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan, Department of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan

Correspondence and reprint requests to: Kunihiro Tsukasaki, Department of Hematology, Molecular Medicine Unit Atomic Bomb Disease Institute Nagasaki University Graduate School of Biomedical Sciences 1-12-4 Sakamoto, Nagasaki, Japan, Tel: +81(95) 849-7111 Fax: +81(95) 849-7113, Email: tsukasak{at}net.nagasaki-u.ac.jp

Lymphoma of the thyroid is almost exclusively derived from B cells of mucosa-associated lymphoid tissue (MALT), and frequently co-exist with autoimmune thyroiditis in which most infiltrating cells are of Th1 cell origin. We present here two rare cases of peripheral T-cell lymphoma (PTCL) based on chronic thyroiditis with the phenotype CD3⁺, CD4⁺, CD8^–, TCRß⁺. Furthermore, lymphoma cells in both cases were CXCR3⁺, CCR5⁺ and ST2(L)^–, suggesting a Th1 cell origin. Eight of 11 cases of PTCL of the thyroid in the literature, including our cases, were associated with thyroiditis. Except for one tumor of T-cell type, all of the five lymphomas analyzed for CD4 expression were positive for the antigen. Among them, both those examined for chemokine receptors were phenotypically of Th1-cell origin with a background of thyroiditis, suggesting that Th1 activation induced by chronic inflammation could lead to PTCL of themselves as well as MALT-lymphoma of B cells.

Key words: T-cell lymphoma, Th1 phenotype, chemokine receptors, autoimmune thyroiditis.