Suzuki K, Tomasi T B
J Immunol. 1980 Oct;125(4):1806-10.
Pretreatment of peritoneal exudate cells (PEC) for 24 to 48 hr with mouse amniotic fluid (MAF) results in a marked reduction in their ability to present antigen in a macrophage-T cell dependent antigen-induced lymphocyte proliferative assay. Since we showed that MAF did not inhibit the uptake of antigen by the antigen-presenting cells, presumably the site of action is either on "processing," T-macrophage interactions and/or on the secretion of soluble factors by macrophages. Whether suppression is the result of a direct effect on MAF on the antigen-presenting cell or indirectly via another cell type present in the PEC preparations was not established by this study. However, our data suggest that a major (although perhaps not sole) site of action of the suppressive factor(s) in MAF is at the level of the antigen-presenting cell. The biologic relevance of these in vitro observations is discussed in regard to the defects of immune function in fetal and neonatal animals.
用小鼠羊水(MAF)对腹腔渗出细胞(PEC)进行24至48小时的预处理,会导致其在巨噬细胞 - T细胞依赖性抗原诱导的淋巴细胞增殖试验中呈递抗原的能力显著降低。由于我们发现MAF并不抑制抗原呈递细胞对抗原的摄取,推测其作用位点可能在“加工”、T细胞与巨噬细胞的相互作用和/或巨噬细胞分泌可溶性因子的过程中。本研究并未确定抑制作用是MAF直接作用于抗原呈递细胞的结果,还是通过PEC制剂中存在的另一种细胞类型间接产生的。然而,我们的数据表明,MAF中抑制因子的主要(尽管可能不是唯一)作用位点位于抗原呈递细胞水平。针对胎儿和新生动物免疫功能缺陷,讨论了这些体外观察结果的生物学相关性。