γδ Τ cells enhance B cells for antibody production in Hashimoto's thyroiditis, and retinoic acid induces apoptosis of the γδ Τ cell.

TCR γδ(+) Τ cells are important in the pathogenesis of inflammatory and autoimmune conditions. This study investigated the effect of γδ T cells on autoantibody production in patients with Hashimoto's thyroiditis (HT). A total of 148 subjects were enrolled, including 99 patients with HT, 5 with simple goiters, and 44 healthy controls. Peripheral blood and thyroid mononuclear cells were subjected to flow cytometric analysis. Thyroid tissues underwent immunofluorescent staining and immunohistochemistry for γδ T cells and anti-thyroid antibody detection. Antibody production was measured by ELISA and automated chemiluminescent immunoassays. And activation and apoptosis of peripheral blood γδT cells and B cells were measured by flow cytometric analysis. The percentage of γδ T cells were greater in thyroid tissue from HT patients than that of goiter patients (n = 5, 5.33 ± 1.20 vs. 2.07 ± 0.44 %; P < 0.05), with the Vδ1(+) γδ T cell subset especially dominant. Frequencies of CD69 (8.42 ± 1.08 vs. 1.60 ± 0.38 %, P < 0.001), HLA-DR (58.12 ± 6.36 vs. 37.82 ± 3.70 %, P < 0.05), CD40L (1.58 ± 0.35 vs. 0.15 ± 0.05 %, P < 0.01), and ICOS (2.78 ± 0.66 vs. 0.28 ± 0.13 %, P < 0.01) expressed on γδ T cells from HT patients (n = 19) were significantly increased compared with those of healthy controls (n = 15). More importantly, γδ T cells from HT patients enhanced B cells for antibody production, and all-trans retinoic acid (ATRA) treatment inhibited the effect by inducing apoptosis of γδ Τ cells. γδ Τ cells appear to play an important role in the pathogenesis of HT, and ATRA might be an effective regulator for HT patients.