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Panayota Kolypetri, George Carayanniotis, Enhanced apoptosis of NOD.H2h4 thyrocytes by low concentrations of iodide: an intrinsic susceptibility factor in iodide-accelerated thyroiditis? (P4148), The Journal of Immunology, Volume 190, Issue Supplement_1, May 2013, Page 172.1, https://doi.org/10.4049/jimmunol.190.Supp.172.1
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Abstract
Enhanced iodide intake in NOD.H2h4 mice accelerates the onset and severity of spontaneous autoimmune thyroiditis (ISAT) via an unknown mechanism. In this study, we have tested two hypotheses: 1) that NOD.H2h4 thyrocytes exhibit increased susceptibility to iodide-mediated apoptosis vs that of thyrocytes from other strains of mice; and 2) that progression of ISAT is associated with a reduction in the number of Treg cells in lymphoid tissues. We report that NOD.H2h4 thyrocytes cultured in vitro for 24 hr with 1-16 μM of NaI exhibited total numbers of apoptotic cells (ranging from 7.2 -32.9% above background) which were significantly higher than similarly treated CBA/J thyrocytes (ranging from 1.5 - 6.3% above background) upon staining with fluorescent caspase inhibitors. In addition, we report that flow cytometry of Treg cells in thyroid-draining lymph nodes (7.6-9.9% of CD4+ cells) or spleens (18.5 -19% of CD4+ cells) of NOD.H2h4 Foxp3-gfp mice did not reveal a significant alteration in their frequency, 7, 11 and 15 days following the initiation of enhanced iodide-intake (0.05 % NaI in drinking water). These results indicate that ISAT is not associated with a decrease of Treg frequency in lymphoid organs during the initial stages of the disease but support the view that an intrinsic high susceptibility of NOD.H2h4 thyrocytes to iodide-mediated apoptosis may be one of the triggering factors in ISAT.