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Hormones (Athens, Greece)

Iodine content of thyroglobulin in Nod.H2h4 mice developing iodine-accelerated autoimmune thyroiditis.


PMID 20687399

Abstract

In NOD.H2h4 mice, high dietary iodine intake has been known to cause iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) via an unknown mechanism. The aim of the study was to examine whether the NOD.H2h4 genetic background predisposes to enhanced iodine organification in thyroglobulin (Tg), a target autoantigen in ISAT. To avoid issues associated with an ongoing anti-Tg antibody response, we assessed Tg iodination levels in iodine-fed, B-cell deficient NOD.H2h4 mice. Additionally, we tested whether humoral or cellular immune responses of iodine-fed NOD.H2h4 mice are preferentially directed to Tg with increased iodine content (I-Tg) or known pathogenic Tg peptides that contained iodine. The iodine content of Tg was not significantly different between control (9.0 +/- 2.7 I atoms per monomer) and iodine-fed mice (10.9 +/- 0.3 I atoms per monomer). Furthermore, in iodine-fed NOD.H2h4 mice developing ISAT, strong but equivalent serum IgG responses were detected to both Tg or I-Tg, whereas their lymphoid cells were stimulated weakly but equally well by Tg or I-Tg in vitro and did not show reactivity against a panel of five pathogenic Tg peptides that contained iodine. The results suggest that development of ISAT in NOD.H2h4 mice is not associated with enhanced iodine organification or differential B- or T-cell responses to iodinated determinants in Tg.