Bolacchi F, Carbone M, Capozzi M, Ventura L, Cepparulo M, Niutta P, Rocchi G, Bergamini A
Department of Public Health and Cellular Biology, Chair of Infectious Diseases, University of Rome Tor Vergata, Rome, Italy.
Cytokine. 2001 Nov 21;16(4):121-5. doi: 10.1006/cyto.2001.0955.
Here we show that CD40L (ligand for CD40) failed to induce the production of tumour necrosis factor alpha (TNF-alpha), interleukin (IL-)-1 beta, IL-10 and IL-12 in macrophages matured in vitro in the absence of growth factors or in the presence of macrophage colony-stimulating factor (M-CSF). In contrast, enzyme-linked immunoabsorbent assay (ELISA) testing and cytofluorimetric (FACS) analysis demonstrated significant production of TNF-alpha and IL-1 beta, but not of IL-10 and IL-12 in macrophages maturated in the presence of CD40L and re-stimulated with CD40L. The priming effect of CD40L on TNF-alpha and IL-1 beta production was related to induction of CD40 expression. Finally, CD40L priming did not modify the cytokine response of macrophages to lipopolysaccharide. In conclusion, our results suggest that CD40/CD40L interactions are important for the activation of macrophages as effector cells that mediate inflammation and tissue damage in T cell-mediated inflammatory processes.
我们在此表明，在无生长因子或存在巨噬细胞集落刺激因子（M-CSF）的情况下体外成熟的巨噬细胞中，CD40L（CD40的配体）未能诱导肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-1β、IL-10和IL-12的产生。相比之下，酶联免疫吸附测定（ELISA）检测和细胞荧光分析（FACS）表明，在存在CD40L并再次用CD40L刺激而成熟的巨噬细胞中，TNF-α和IL-1β有显著产生，但IL-10和IL-12没有。CD40L对TNF-α和IL-1β产生的启动作用与CD40表达的诱导有关。最后，CD40L启动并未改变巨噬细胞对脂多糖的细胞因子反应。总之，我们的结果表明，CD40/CD40L相互作用对于巨噬细胞作为效应细胞的激活很重要，这些效应细胞在T细胞介导的炎症过程中介导炎症和组织损伤。
