Supplementary Material for: Expression of the Inhibitory CD200 Receptor Is Associated with Alternative Macrophage Activation

Classical macrophage activation is inhibited by the CD200 receptor (CD200R). Here, we show that CD200R expression was specifically induced on human in vitro polarized macrophages of the alternatively activated M2a subtype, generated by incubation with IL-4 or IL-13. In mice, peritoneal M2 macrophages, elicited during infection with the parasites <i>Taenia crassiceps</i> or <i>Trypanosoma brucei brucei</i>, expressed increased CD200R levels compared to those derived from uninfected mice. However, in vitrostimulation of mouse peritoneal macrophages and <i>T. crassiceps</i> infection in IL-4–/– and IL-4R–/– mice showed that, in contrast to humans, induction of CD200R in mice was not IL-4 or IL-13 dependent. Our data identify CD200R as a suitable marker for alternatively activated macrophages in humans and corroborate observations of distinct species- and/or site-specific mechanisms regulating macrophage polarization in mouse and man.

CD200受体（CD200R）可抑制经典巨噬细胞活化。本研究发现，在经白细胞介素-4（IL-4）或白细胞介素-13（IL-13）诱导的体外极化人交替活化M2a亚型巨噬细胞中，CD200R的表达被特异性上调。在小鼠体内，感染粗尾带绦虫（*Taenia crassiceps*）或布氏布氏锥虫（*Trypanosoma brucei brucei*）时诱导产生的腹膜M2巨噬细胞，其CD200R表达水平较未感染小鼠来源的巨噬细胞显著升高。然而，对小鼠腹膜巨噬细胞进行体外刺激，以及在IL-4基因敲除（IL-4–/–）和IL-4受体基因敲除（IL-4R–/–）小鼠中感染*T. crassiceps*的实验结果表明，与人类不同，小鼠体内CD200R的诱导并不依赖IL-4或IL-13。本研究明确CD200R可作为人交替活化巨噬细胞的特异性标志物，并证实了调控小鼠与人类巨噬细胞极化的机制存在显著的物种和/或位点特异性差异。