Buisman A, van Dissel J T, Langermans J A, van Furth R
Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
Infect Immun. 1994 Mar;62(3):1121-4. doi: 10.1128/iai.62.3.1121-1124.1994.
The induction of reactive nitrogen intermediates (RNI) and toxoplasmastatic activity of murine macrophages by recombinant gamma interferon (rIFN-gamma) is mediated by an autocrine pathway involving tumor necrosis factor alpha (TNF-alpha). To investigate whether cytokines other than TNF-alpha play a role in the activation of these effector functions, granulocyte-macrophage colony-stimulating factor (GM-CSF) was studied. Recombinant GM-CSF (rGM-CSF) could stimulate peritoneal macrophages, since this cytokine stimulated the production of prostaglandin E2 by these cells. However, rGM-CSF did not induce either the release of RNI by or the toxoplasmastatic activity of macrophages. rGM-CSF in combination with various concentrations of rIFN-gamma did not enhance these effector functions more than rIFN-gamma alone. Furthermore, neutralization of endogenously produced GM-CSF by monoclonal antibodies did not affect the release of RNI by or the toxoplasmastatic activity of rIFN-gamma-activated macrophages. Together these results indicate that GM-CSF is not involved in RNI production by and toxoplasmastatic activity of IFN-gamma-activated murine macrophages.
重组γ干扰素（rIFN-γ）诱导小鼠巨噬细胞产生反应性氮中间产物（RNI）及抑制弓形虫活性是通过一条涉及肿瘤坏死因子α（TNF-α）的自分泌途径介导的。为了研究除TNF-α之外的细胞因子是否在这些效应功能的激活中发挥作用，对粒细胞-巨噬细胞集落刺激因子（GM-CSF）进行了研究。重组GM-CSF（rGM-CSF）能够刺激腹腔巨噬细胞，因为这种细胞因子能刺激这些细胞产生前列腺素E2。然而，rGM-CSF既不诱导巨噬细胞释放RNI，也不诱导其产生抑制弓形虫活性。rGM-CSF与不同浓度的rIFN-γ联合使用，对这些效应功能的增强作用并不比单独使用rIFN-γ更强。此外，用单克隆抗体中和内源性产生的GM-CSF并不影响rIFN-γ激活的巨噬细胞释放RNI或其抑制弓形虫活性。这些结果共同表明，GM-CSF不参与IFN-γ激活的小鼠巨噬细胞产生RNI及抑制弓形虫活性的过程。
