caa a22 4500 465805833 CHVBK 20180323112103.0 cr unu---uuuuu 170327e19901201xx s 000 0 eng 10.1007/BF03349645 doi (NATIONALLICENCE)springer-10.1007/BF03349645 Effects of recombinant human interferon gamma on human thyroid tissues from patients with Graves' disease and normal subjects transplanted into nude mice [Elektronische Daten] [Y. Kasuga, S. Matsubayashi, Y. Sakatsume, N. Miller, C. Jamieson, R. Volpé] 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 IFNγ(hlFNγ) 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) HLA-DR 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 HLA-DR 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 HLA-DR 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. Italian Society of Endocrinology (SIE), 1990 Nude mice nationallicence interferon gamma nationallicence Graves' disease nationallicence xenografts nationallicence Kasuga Y. Wellesley Hospital Research Foundation, Canada aut Matsubayashi S. Angus Foundation, The Wellesley Hospital, Canada aut Sakatsume Y. Angus Foundation, The Wellesley Hospital, Canada aut Miller N. Department of Medicine, Pathology, The Wellesley Hospital, University of Toronto, Toronto, Ontario, Canada aut Jamieson C. University of Toronto, Toronto, Ontario, Canada aut Volpé R. Endocrinology Research Laboratory and Department of Medicine, The Wellesley Hospital, 160 Wellesley Street East, M4Y IJ3, Toronto, Ontario, Canada aut Journal of Endocrinological Investigation Springer International Publishing 13/11(1990-12-01), 871-878 0391-4097 13:11<871 1990 13 40618 https://doi.org/10.1007/BF03349645 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF03349645 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Kasuga Y. Wellesley Hospital Research Foundation, Canada aut NATIONALLICENCE 700 1- Matsubayashi S. Angus Foundation, The Wellesley Hospital, Canada aut NATIONALLICENCE 700 1- Sakatsume Y. Angus Foundation, The Wellesley Hospital, Canada aut NATIONALLICENCE 700 1- Miller N. Department of Medicine, Pathology, The Wellesley Hospital, University of Toronto, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Jamieson C. University of Toronto, Toronto, Ontario, Canada aut NATIONALLICENCE 700 1- Volpé R. Endocrinology Research Laboratory and Department of Medicine, The Wellesley Hospital, 160 Wellesley Street East, M4Y IJ3, Toronto, Ontario, Canada aut NATIONALLICENCE 773 0- Journal of Endocrinological Investigation Springer International Publishing 13/11(1990-12-01), 871-878 0391-4097 13:11<871 1990 13 40618 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer