Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114.
John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138.
Proc Natl Acad Sci U S A. 2020 Sep 22;117(38):23336-23338. doi: 10.1073/pnas.1922788117. Epub 2020 Sep 8.
Colony-stimulating factor 1 receptor (CSF1R) inhibition has been proposed as a method for microglia depletion, with the assumption that it does not affect peripheral immune cells. Here, we show that CSF1R inhibition by PLX5622 indeed affects the myeloid and lymphoid compartments, causes long-term changes in bone marrow-derived macrophages by suppressing interleukin 1β, CD68, and phagocytosis but not CD208, following exposure to endotoxin, and also reduces the population of resident and interstitial macrophages of peritoneum, lung, and liver but not spleen. Thus, small-molecule CSF1R inhibition is not restricted to microglia, causing strong effects on circulating and tissue macrophages that perdure long after cessation of the treatment. Given that peripheral monocytes repopulate the central nervous system after CSF1R inhibition, these changes have practical implications for relevant experimental data.
集落刺激因子 1 受体 (CSF1R) 抑制被提议作为一种小胶质细胞耗竭的方法,其假设是它不会影响外周免疫细胞。在这里,我们表明 PLX5622 确实通过抑制白细胞介素 1β、CD68 和吞噬作用但不抑制 CD208 来抑制 CSF1R,从而影响骨髓来源的巨噬细胞的髓系和淋巴系,这会导致暴露于内毒素后长期变化,也会减少腹膜、肺和肝的驻留和间质巨噬细胞的数量,但不会减少脾的驻留和间质巨噬细胞的数量。因此,小分子 CSF1R 抑制不仅限于小胶质细胞,它会对循环和组织巨噬细胞产生强烈影响,并且在治疗停止后很长时间仍会持续。鉴于外周单核细胞在 CSF1R 抑制后会重新填充中枢神经系统,这些变化对相关实验数据具有实际意义。