Axelsson J A, Källén B
Z Immunitatsforsch Immunobiol. 1976 Sep;152(2):167-77.
Rats of certain strains immunized with bovine encephalitogenic protein (EP) in Freund's complete adjuvant develop an impairment of the mixed leukocyte reaction (MLR) similar to that seen in rabbits with experimental autoimmune encephalomyelitis and in humans with certain diseases, including multiple sclerosis. The rats mount a cell-bound response to EP, but encephalomyelitis does not develop. The component causing the impairment was analysed in a culture system using inbred rat strains and F1 hybrids, thoracic duct cells as a source of lymphocytes, and blood as a supplement to the cultures. In normal rats, it was shown that the effects of responding and of stimulating lymphocytes could be separated and that the supportive action of the added blood was probably due to macrophages (monocytes); also that the added blood could in many experiments be replaced with 2-mercaptoethanol (2-ME). The impairment present in immunized rats is at least largely due to a defective supportive activity of the blood (monocytes) and can be restored with 2-ME. The results argue that the MLR impairment seen in immunized rats is due to a faulty macrophage function.
用弗氏完全佐剂中的牛致脑炎蛋白（EP）免疫特定品系的大鼠，会出现混合淋巴细胞反应（MLR）受损，这与实验性自身免疫性脑脊髓炎的兔子以及包括多发性硬化症在内的某些疾病的人类中所见的情况相似。这些大鼠对EP产生细胞结合反应，但不会发生脑脊髓炎。在一个培养系统中，使用近交系大鼠品系和F1杂种、胸导管细胞作为淋巴细胞来源以及血液作为培养补充物，对导致这种损伤的成分进行了分析。在正常大鼠中，结果表明反应性淋巴细胞和刺激性淋巴细胞的作用可以分开，并且添加血液的支持作用可能归因于巨噬细胞（单核细胞）；此外，在许多实验中，添加的血液可以用2-巯基乙醇（2-ME）替代。免疫大鼠中存在的损伤至少在很大程度上归因于血液（单核细胞）的支持活性缺陷，并且可以用2-ME恢复。结果表明，免疫大鼠中所见的MLR损伤是由于巨噬细胞功能异常所致。
