L'involution de l'hyperplasie thyroïdienne chez la souris c3h

Thèse de doctorat -- Université catholique de Louvain, 198

Iodine and goiter involution.

Iodine administration, although efficient in goiter treatment or prevention, is also responsible for adverse effects such as cell necrosis or thyroiditis. These two effects were reproduced in iodide-treated goitrous mice. Morphological observations strongly suggest that thyroid cell death results from an excessive production of free radicals, which initiates lipid peroxidation. This hypothesis is strengthened by the facts that the thyroidal concentration of malonic dialdehyde, a stable product of lipid peroxidation, is increased, and that necrosis is partially prevented by free radicals scavengers. Epithelial necrosis is associated to an inflammatory reaction. The infiltrate is mainly made of cells expressing class II molecules of major histocompatibility complex (macrophages and dendritic cells), but also of T lymphocytes. However, this inflammation, which varies among mouse strains, is transient and it is not amplified or maintained by administration of cytokines, IFN gamma or TNF alpha, known to induce class II expression on thyrocytes

The autoimmune thyroid disease induced by immunising mice with recombinant human thyrotropin receptor varies with the genetic background.

info:eu-repo/semantics/nonPublishe

Transfer of thyroiditis with spleen cells from mice immunised with recombinant human thyrotropin receptor (TSHR)

info:eu-repo/semantics/nonPublishe

La goitrigenèse expérimentale.

Various modern aspects of experimental goitrogenesis are reviewed and discussed. Regulation of follicular cell proliferation clearly involves several stimulatory but also inhibitory mechanisms. Furthermore, different stimuli are probably involved. Growth of the vascular and connective interstitial tissue probably involves paracrine factors and that of the follicles maybe autocrine factors; indeed, several growth factors are secreted by stimulated follicular cells. The formation of nodules is still poorly understood. They could derive from different cell populations or from cells being in different reactivity status with respect to the variations of the iodine fluxes in the gland. Finally, the relationship between iodine toxicity, nodularity and autoimmunity are discussed