Identification of a common gene signature for type H cytokine-associated myeloid cells elicited in vivo in different pathologic conditions
Identification of a common gene signature for type H cytokine-associated myeloid cells elicited in vivo in different pathologic conditions
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DOI：
10.1182/blood-2005-04-1485
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发表时间：
2006-07-15
期刊：
影响因子：
20.3
通讯作者：
Raes, Geert
中科院分区：
文献类型：
--
作者：
Ghassabeh, Gholamreza Hassanzadeh;De Baetselier, Patrick;Raes, Geert
与I型细胞因子相关髓样细胞（M1）相比，II型细胞因子相关髓样细胞（M2）的分子库和功能特性的机制尚不清楚。此外，大多数研究仅限于体外诱导的M2细胞。在这里，在寄生虫感染和癌症的小鼠模型中，M1和M2细胞的比较基因表达谱得出了独立于疾病模型、小鼠品系和细胞器官来源的体内诱导M2群体的共同特征。其中一些基因，如钙粘蛋白-1、硒蛋白P、血小板活化因子乙酰水解酶和丙苷，尚未被证实与M2相关。总的来说，这些共同的特征基因为M2的一些已知或建议的特性提供了分子基础，包括免疫调节、炎症下调、抗氧化损伤、高吞噬能力和组织修复。有趣的是，一些常见的M2特征基因编码膜相关标记，可能对M2的鉴定和分离有用。其中一些基因在各种体外环境下不能被IL-4/IL-13或IL-10诱导，因此在基于体外活化细胞的方法中被遗漏，验证了我们选择的骨髓细胞表达谱的体内模型。
Compared with type I cytokine-associated myeloid (M1) cells, the molecular repertoire and mechanisms underlying functional properties of type II cytokine-associated myeloid (M2) cells are poorly characterized. Moreover, most studies have been limited to in vitro-elicited M2 cells. Here, comparative gene expression profiling of M1 and M2 cells, elicited in murine models of parasitic infections and cancer, yielded a common signature for in vivo-induced M2 populations independent of disease model, mouse strain, and organ source of cells. Some of these genes, such as cadherin-1, selenoprotein P, platelet-activating factor acetylhydrolase, and prosaposin, had not been documented as associated with M2. Overall, the common signature genes provide a molecular basis for a number of documented or suggested properties of M2, including immunomodulation, downregulation of inflammation, protection against oxidative damage, high capacity for phagocytosis, and tissue repair. Interestingly, several common M2 signature genes encode membrane-associated markers that could be useful for the identification and isolation of M2. Some of these genes were not induced by IL-4/IL-13 or IL-10 under various in vitro settings and thus were missed in approaches based on in vitro-activated cells, validating our choice of in vivo models for expression profiling of myeloid cells.