Kasai K, Banba N, Motohashi S, Fukuda H, Manaka K, Matsumura M, Sekiguchi Y, Hattori Y
Department of Endocrinology, Internal Medicine, Dokkyo University School of Medicine, Tochigi, Japan.
Biochem Biophys Res Commun. 1997 Sep 8;238(1):191-6. doi: 10.1006/bbrc.1997.7244.
Monocytes/macrophages can be activated by the colony-stimulating factors (CSFs), granulocyte/macrophage CSF and macrophage CSF, and play a pivotal role in immune and inflammatory responses. We examined whether human thyrocytes can produce these CSFs. Interleukin-1 (IL-1) strongly up-regulated the gene and protein expression of the two CSFs. Interferon-gamma stimulated M-CSF expression but inversely suppressed GM-CSF expression in either basal or IL-1-stimulated condition. Thyrocytes prepared from Graves' thyroid tissues produced relatively larger amounts of GM-CSF in response to IL-1 and M-CSF in both basal and IL-1-stimulated conditions when compared to those obtained from normal and adenomatous goiter thyroid tissues. Thyrotropin attenuated M-CSF, but not GM-CSF, production. The present finding indicates that human thyrocytes themselves produce both GM-CSF and M-CSF, and thus may participate in immune and inflammatory responses through these CSFs production.
单核细胞/巨噬细胞可被集落刺激因子（CSF）、粒细胞/巨噬细胞集落刺激因子和巨噬细胞集落刺激因子激活，并在免疫和炎症反应中起关键作用。我们研究了人类甲状腺细胞是否能产生这些集落刺激因子。白细胞介素-1（IL-1）强烈上调了这两种集落刺激因子的基因和蛋白表达。在基础状态或IL-1刺激状态下，干扰素-γ刺激巨噬细胞集落刺激因子（M-CSF）表达，但却反向抑制粒细胞/巨噬细胞集落刺激因子（GM-CSF）表达。与从正常和腺瘤性甲状腺肿甲状腺组织获得的甲状腺细胞相比，从格雷夫斯甲状腺组织制备的甲状腺细胞在基础状态和IL-1刺激状态下对IL-1和M-CSF的反应中产生相对大量的GM-CSF。促甲状腺激素减弱M-CSF的产生，但不减弱GM-CSF的产生。目前的发现表明，人类甲状腺细胞自身产生GM-CSF和M-CSF，因此可能通过这些集落刺激因子的产生参与免疫和炎症反应。
