Clodronate liposomes 由包封在磷脂双分子层脂质体内的氯磷酸盐组成，可以被巨噬细胞选择性摄取。在巨噬细胞溶酶体内，磷酸酶逐步释放脂质体内的氯磷酸盐，使其在细胞内累积。当达到阈值浓度时，该累积会导致巨噬细胞不可逆损伤并诱导凋亡，使 clodronate liposomes 成为研究巨噬细胞清除及免疫调控的重要工具。Clodronate liposomes是荷兰免疫学家Nico Van Rooijen在上世纪90年代发明开发。Nico Van Rooijen为Clodronate liposomes清除巨噬细胞做了很多原创性，基础性的工作，发表了大量文献。
当使用荷兰Liposoma的巨噬细胞清除剂Clodronate liposomes氯膦酸盐脂质体，气管给药清除肺部肺泡巨噬细胞细胞时，巨噬细胞清除剂氯膦酸盐脂质体Clodronate liposomes会清除DC细胞吗？肺泡巨噬细胞和DC细胞都是CD11c阳性，根据如下文献的研究，气管内给药Clodronate liposomes不会清除DC细胞。
文献题目：Murine alveolar macrophages limit replication of vaccinia virus
动物品系：129 Ev/Sv小鼠
给药方法：气管注射100 uL
原文描述：
Some populations of dendritic cells may be depleted by clodronate liposomes (Leenen et al., 1998), although effects of this treatment on lung dendritic cells remain poorly defined. We quantified numbers of dendritic cells in lungs of mice treated with clodronate or control saline liposomes. Clodronate liposomes did not affect total numbers of CD11c(+), MHC class II(+) dendritic cells in the lung interstitium as compared with control liposomes. In both groups, dendritic cells comprised ≈ 0.8% of total cells in the lungs, which is consistent with our previous data from untreated mice. Because antigen presenting cells such as dendritic cells and macrophages migrate to regional lymph nodes to initiate adaptive immunity, we also quantified numbers of these cell types in the tracheobronchial lymph node of mice 2 days after injection of liposomes. There were no significant differences between clodronate and saline control mice in numbers or percentages of CD11c(+), MHC class II(+) dendritic cells, Mac-3(+) macrophages, or ERMP-20(+) late monocyte progenitors in these lymph nodes (data not shown). Furthermore, numbers or percentages of dendritic cells and macrophages in peripheral blood, as determined by these same cell surface markers, did not differ between mice 2 days following treatment with clodronate or saline liposomes (data not shown). Collectively, these data demonstrate that intratracheal administration of clodronate liposomes depleted only alveolar macrophages.
原文翻译：
某些群体的树突状细胞可能会被氯膦酸盐脂质体消耗（Leenen 等，1998），尽管这种处理对肺树突状细胞的影响尚不清楚。我们对接受氯膦酸盐脂质体或对照生理盐水脂质体处理的小鼠肺部树突状细胞数量进行了量化。与对照脂质体相比，氯膦酸盐脂质体并未影响肺间质中 CD11c(+ )、MHC II(+ ) 树突状细胞的总数。在两组中，树突状细胞约占肺总细胞的 0.8%，这与我们之前在未经处理的小鼠中获得的数据一致。由于抗原呈递细胞如树突状细胞和巨噬细胞会迁移至区域淋巴结以启动适应性免疫，我们还量化了脂质体注射后 2 天小鼠气管支气管淋巴结中这些细胞类型的数量。氯膦酸盐脂质体与生理盐水对照小鼠在气管支气管淋巴结中 CD11c(+ )、MHC II( +) 树突状细胞、Mac-3(+ ) 巨噬细胞或 ERMP-20( +) 晚期单核细胞前体的数量或百分比之间没有显著差异（数据未显示）。此外，通过这些相同的细胞表面标志确定的外周血中树突状细胞和巨噬细胞的数量或百分比，在氯膦酸盐脂质体或生理盐水脂质体处理后 2 天的小鼠之间也无差异（数据未显示）。总体而言，这些数据表明，气管内给予氯膦酸盐脂质体仅能消耗肺泡巨噬细胞。
参考文献：
P. Leenen et al., Heterogeneity of mouse spleen dendritic cells: in vivo phagocytic activity, expression of macrophage markers, and subpopulation turnover. J. Immunol., 160 (5) (1998), pp. 2166-2173.
