Ansfield M J, Benson B J
J Immunol. 1980 Sep;125(3):1093-8.
Pulmonary surface active material (SAM), purified from canine lung lavage fluids, is a phospholipid-rich lipoprotein with potent immunosuppressive activity. Experiments were performed to identify those components of SAM that were responsible for this immunosuppressive effect. Results indicated that the lipid, and not the protein, fraction of SAM was immunosuppressive. Two phospholipids, phosphatidylglycerol and phosphatidylcholine, were identified as the predominant immunosuppressive components of the SAM-lipid fraction. lymphocyte proliferation in response to mitogenic or allogeneic stimulation was suppressed by intact SAM, SAM-lipid, phosphatidylglycerol, and phosphatidylcholine. Each of these preparations inhibited RNA, protein and DNA synthesis by mitogen-stimulated lymphocytes. Antioxidants consistently failed to diminish the immunosuppressive properties of SAM or its lipid components. The mechanism of this immunosuppressive action of SAM and its phospholipid components remains undefined. Our data indicate, however, that it is unlikely to be due either to cytotoxicity or to an artifact of lipid oxidation in vitro.
从犬肺灌洗液中纯化得到的肺表面活性物质（SAM）是一种富含磷脂的脂蛋白，具有强大的免疫抑制活性。进行了实验以确定SAM中导致这种免疫抑制作用的成分。结果表明，SAM的脂质部分而非蛋白质部分具有免疫抑制作用。两种磷脂，磷脂酰甘油和磷脂酰胆碱，被确定为SAM脂质部分的主要免疫抑制成分。完整的SAM、SAM脂质、磷脂酰甘油和磷脂酰胆碱均可抑制淋巴细胞对有丝分裂原或同种异体刺激的增殖。这些制剂中的每一种都能抑制有丝分裂原刺激的淋巴细胞的RNA、蛋白质和DNA合成。抗氧化剂始终无法削弱SAM或其脂质成分的免疫抑制特性。SAM及其磷脂成分这种免疫抑制作用的机制尚不清楚。然而，我们的数据表明，这不太可能是由于细胞毒性或体外脂质氧化的假象所致。
