ADJUVANT POLYARTHRITIS .4. INDUCTION BY A SYNTHETIC ADJUVANT - IMMUNOLOGICAL, HISTOPATHOLOGIC, AND OTHER STUDIES

ADJUVANT POLYARTHRITIS .4. INDUCTION BY A SYNTHETIC ADJUVANT - IMMUNOLOGICAL, HISTOPATHOLOGIC, AND OTHER STUDIES
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DOI:
10.1002/art.1780230111
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发表时间:
1980-01-01
影响因子:
--
通讯作者:
ABE, C
ABE, C
中科院分区:
其他
文献类型:
--
作者:
CHANG, YH;PEARSON, CM;ABE, C

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将明显非免疫原性的合成化合物 N,N-双十八烷基-N'',N''-双(2-羟乙基)丙二胺 (CP-20961) 悬浮在矿物油或橄榄油 (50 mg/ml) 中的溶液,在 Lewis 大鼠的尾部或后爪进行单次皮内注射 (0.2 ml) 时,可诱发急性、慢性多关节炎。多关节炎在形态上与弗氏完全佐剂(FCA)诱导的经典佐剂关节炎几乎没有区别,这种疾病通常被认为是对注射的结核杆菌成分产生迟发性超敏反应的结果。 CP-20961诱导的疾病和弗氏完全佐剂诱导的疾病遵循相同的时间进程和几乎相同的临床和组织病理学特征的发展模式。与经典的佐剂性关节炎一样,CP-20961 诱导的关节炎可以通过免疫抑制剂(环磷酰胺)或抗炎药(保泰松)来抑制。烷基二胺 (CP-20961) 是有效的佐剂;腹膜内施用的化合物在矿物油中的分散体或溶液。增强了大鼠体内针对[小鼠白血病]EL4细胞的细胞介导和体液免疫反应的发展。导致佐剂关节炎发生的免疫原显然是内源性的,例如宿主组织的成分、病毒蛋白或两者的某种复合物。
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 acute, chronic polyarthritis when single intradermal injections (0.2 ml) were made in the tail or hindpaw of Lewis rat. 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 potent adjuvant; a dispersion or solution of the compound in mineral oil administered i.p. enhanced the development of the cell-mediated and the humoral immune responses to [mouse leukemia] EL4 cells in the rat. The immunogen responsible for development of adjuvant arthritis is apparently endogenous, e.g., a constituent of host tissue, a viral protein or some complex of the 2.