Authors: Y Kasuga S Matsubayashi Y Sakatsume N Miller C Jamieson R Volpé
Publish Date: 2014/04/09
Volume: 13, Issue: 11, Pages: 871-878
Abstract
We have attempted to determine whether interferon gamma IFNγ would enhance sustain or induce autoimmune thyroid disease AITD in xenotransplanted thyroid tissue from patients with Graves’ disease or normal persons actually paranodular tissue in nude athymic mice in the absence of an intact immune system A dosage of 4000 U/mouse of human IFNγhlFNγ was injected intraperitoneally daily for six consecutive weeks into the xenotransplanted mice The parameters measured included the free T4 index thyroid autoantibodies and TSH during the course of hlFNγ injections Thyroid epithelial cell TEC HLADR expression was measured in the thyroid tissue before xenotransplantation and at sacrifice in addition light and electron microscopic studies were carried out at those times There were no significant differences in thyroid function between the control results and those obtained with hlFNγ in either group of tissues TEC HLADR expression was significantly increased by hlFNγ in the normal group but insignificantly in the Graves’ group In both light and electron microscopic observations Graves’ tissue whether or not treated with hlFNγ was indistinguishable at sacrifice from normal thyroid tissue The appearance had markedly altered from the same Graves’ tissue examined at the time of the initial human surgery which then showed the usual histological appearance of this disorder We conclude that IFNγ induced HLADR expression alone is not sufficient to sustain the ongoing process of AITD in this model Graves’ TEC appear to be essentially normal when removed from their immune environment it may be proposed that TEC may be mere passive captives to immunologic events in terms of the pathogenesis of AITD without any intrinsic functional abnormality
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