Vecchiarelli A, Puliti M, Torosantucci A, Cassone A, Bistoni F
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.
Cell Immunol. 1991 Apr 15;134(1):65-76. doi: 10.1016/0008-8749(91)90331-5.
Mannoprotein components from Candida albicans were investigated for their ability to induce production of tumor necrosis factor (TNF) by cultured splenocytes from naive or Candida-infected mice. Two chromatographically separated mannoproteins preparations, designated F1 and F2, were as able as the heat-inactivated Candida cells to induce the production of TNF from splenocytes of naive animals. In addition, they caused a significant augmentation of basic TNF secretion by splenocytes of Candida-infected animals. Experiments using plastic and/or nylon wool adherence, as well as treatments with antibodies depleting T or NK cells, consistently indicated that most if not all TNF was produced by splenic macrophages. In cultures of splenocytes from Candida-infected mice, mannoprotein addition also stimulated interferon-gamma (IFN-gamma) production by Thy 1.2 positive cells. Depletion of these cells or addition of anti-IFN-gamma antibodies abolished IFN production and reduced TNF secretion by adherent cells to the levels found in the cultures of mannoprotein-stimulated spleen cells from naive mice. These data add further evidence to the immunomodulatory properties possessed by some cell wall constituents of the human commensal microorganism C. albicans and suggest that IFN-gamma is endowed with a regulatory role in TNF production by mouse macrophages in vitro.
对白色念珠菌的甘露糖蛋白成分进行了研究，以考察其诱导未感染或已感染念珠菌的小鼠脾脏细胞产生肿瘤坏死因子（TNF）的能力。两种经色谱分离的甘露糖蛋白制剂，分别命名为F1和F2，其诱导未感染动物脾脏细胞产生TNF的能力与热灭活的念珠菌细胞相当。此外，它们还显著增强了已感染念珠菌动物脾脏细胞的基础TNF分泌。使用塑料和/或尼龙毛黏附实验，以及用抗体清除T细胞或NK细胞的处理方法，均一致表明，大部分（如果不是全部）TNF是由脾脏巨噬细胞产生的。在已感染念珠菌的小鼠脾脏细胞培养物中，添加甘露糖蛋白还刺激了Thy 1.2阳性细胞产生γ干扰素（IFN-γ）。清除这些细胞或添加抗IFN-γ抗体可消除IFN的产生，并使黏附细胞的TNF分泌降低至未感染小鼠的甘露糖蛋白刺激脾脏细胞培养物中的水平。这些数据进一步证明了人类共生微生物白色念珠菌的某些细胞壁成分具有免疫调节特性，并表明IFN-γ在体外对小鼠巨噬细胞产生TNF具有调节作用。
