Chang Y H, Pearson C M, Abe C
Arthritis Rheum. 1980 Jan;23(1):62-71. doi: 10.1002/art.1780230111.
A solution of an apparently nonimmunogenic synthetic compound, N,N-dioctadecyl-N',N'-bis(2-hydroxyethyl) propanediamine (CP-20961), suspended in mineral oil or olive oil (50 mg/ml), induced an acute, as well as a chronic, polyarthritis when single intradermal injections (0.2 ml) were made in the tail or hindpaw of Lewis rats. The polyarthritis was morphologically almost indistinguishable from classic adjuvant arthritis induced by Freund's complete adjuvant (FCA), a disease generally thought to be the result of a delayed hypersensitivity reaction to a constituent(s) of the injected tubercle bacilli. The disease induced by CP-20961 and that induced by Freund's complete adjuvant followed the same time course and almost identical pattern of development of clinical and histopathologic features. Like the classic adjuvant arthritis, CP-20961 induced arthritis is suppressed by an immunosuppressive agent (cyclophosphamide) or an antiinflammatory drug (phenylbutazone). The alkyldiamine (CP-20961) was found to be a potent adjuvant; a dispersion or a solution of the compound in mineral oil administered intraperitoneally enhanced the development of both the cell-mediated and the humoral immune responses to EL4 cells in the rat. These findings suggest that the immunogen responsible for the development of adjuvant arthritis is endogensou, e.g., a constituent of host tissue, a viral protein, or some complex of the two.
一种明显无免疫原性的合成化合物N,N-二十八烷基-N',N'-双(2-羟乙基)丙烷二胺(CP-20961)悬浮于矿物油或橄榄油(50毫克/毫升)中的溶液，当在Lewis大鼠的尾部或后爪进行单次皮内注射(0.2毫升)时，会诱发急性和慢性多关节炎。这种多关节炎在形态学上与弗氏完全佐剂(FCA)诱发的经典佐剂性关节炎几乎无法区分，FCA诱发的疾病一般被认为是对注射的结核杆菌成分的迟发型超敏反应的结果。CP-20961诱发的疾病和弗氏完全佐剂诱发的疾病具有相同的病程以及几乎相同的临床和组织病理学特征发展模式。与经典佐剂性关节炎一样，CP-20961诱发的关节炎可被免疫抑制剂(环磷酰胺)或抗炎药(保泰松)抑制。发现烷基二胺(CP-20961)是一种有效的佐剂；该化合物在矿物油中的分散液或溶液腹腔内给药可增强大鼠对EL4细胞的细胞介导免疫反应和体液免疫反应的发展。这些发现表明，负责佐剂性关节炎发展的免疫原是内源性的，例如宿主组织的一种成分、一种病毒蛋白或两者的某种复合物。
