Orlikowsky T, Wang Z Q, Dudhane A, Horowitz H, Conti B, Hoffmann M K
New York Medical College, Department of Microbiology, Valhalla 10595, USA.
Immunology. 1997 May;91(1):104-8. doi: 10.1046/j.1365-2567.1997.00204.x.
Forming cellular conjugates with T cells, macrophages can help their targets to mount an immune response or they can destroy the targeted T cell. The two functions are performed by two distinct macrophage subsets that can be distinguished by cell surface marker phenotypes, B7+ CD16- and B7- CD16+. Interferon-gamma (IFN-gamma) induces the former, interleukin-10 (IL-10) induces the latter phenotype. The two macrophage differentiation pathways are mutually exclusive; each cytokine inhibits the effect of the other cytokine. The second messenger cAMP enhances the macrophage B7 expression and suppresses the macrophage CD16 expression. However, together with IL-10, cAMP blocks the generation of both macrophage phenotypes. In the chimpanzee we noted deviations from this differentiation pattern that are suggestive of an enhanced IL-10 presence in the primate environment.
巨噬细胞与T细胞形成细胞共轭体后,可帮助其靶标产生免疫反应,也可破坏被靶向的T细胞。这两种功能由两个不同的巨噬细胞亚群执行,可通过细胞表面标志物表型B7 + CD16 - 和B7 - CD16 + 进行区分。干扰素 - γ(IFN - γ)诱导前者,白细胞介素 - 10(IL - 10)诱导后者表型。这两条巨噬细胞分化途径相互排斥;每种细胞因子都会抑制另一种细胞因子的作用。第二信使cAMP增强巨噬细胞B7表达并抑制巨噬细胞CD16表达。然而,cAMP与IL - 10一起会阻断两种巨噬细胞表型的产生。在黑猩猩中,我们注意到这种分化模式存在偏差,这表明在灵长类动物环境中IL - 10的存在有所增强。