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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Toll-like receptor-MyD88 and Fc receptor pathways of mast cells mediate the thyroid dysfunctions observed during nonthyroidal illness
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Toll-like receptor-MyD88 and Fc receptor pathways of mast cells mediate the thyroid dysfunctions observed during nonthyroidal illness

机译：肥大细胞的Toll样受体MyD88和Fc受体通路介导在非甲状腺疾病期间观察到的甲状腺功能障碍

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摘要

Bacterial infections and other pathologic conditions induce complex dysfunctions of the hypothalamic-pituitary-thyroid axis, collectively known as nonthyroidal illness (NTI). To explore the pathogenesis of bacterial NTI, we injected Mycobacterium tuberculosis extracts or Escherichia coli LPS in mice lacking key components of the Toll-like receptor or crystallizable fragment (Fc) receptor pathways. In wild-type mice, the bacterial components induced a hypothyroidism characterized by elements of both hypothalamic and thyroidal dysfunction. This NTI hypothyroidism did not develop in mice lacking the MyD88 adaptor or in those with a reduced number of mast cells. The hypothyroid responsiveness to LPS, however, was restored upon reconstitution with mast cells derived from the bone marrow of wild-type donors. In addition to bacterial components, whole immunoglobulins induced NTI hypothyroidism in wild-type mice, but not in those lacking activating Fc receptors or mast cells. The study demonstrates a link between Toll-like and Fc receptor signaling and thyroid gland function, uncovering a role of mast cells in murine NTI.
机译：细菌感染和其他病理状况会诱发下丘脑-垂体-甲状腺轴的复杂功能障碍，统称为非甲状腺疾病（NTI）。为了探索细菌NTI的发病机理，我们在缺乏Toll样受体或可结晶片段（Fc）受体途径关键成分的小鼠中注射了结核分枝杆菌提取物或大肠杆菌LPS。在野生型小鼠中，细菌成分诱发甲状腺功能低下，其特征是下丘脑和甲状腺功能障碍的要素。在缺乏MyD88接头的小鼠或肥大细胞数量减少的小鼠中，不会出现这种NTI甲状腺功能减退症。然而，用野生型供体骨髓来源的肥大细胞重建后，对LPS的甲状腺功能减退反应得以恢复。除了细菌成分外，整个免疫球蛋白还可以在野生型小鼠中诱发NTI甲状腺功能减退，但在缺乏激活性Fc受体或肥大细胞的小鼠中则不会。该研究证明了Toll样和Fc受体信号传导与甲状腺功能之间的联系，揭示了肥大细胞在鼠NTI中的作用。

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