Hanauske-Abel H M, Pontz B F, Schorlemmer H U
Ann Rheum Dis. 1982 Apr;41(2):168-76. doi: 10.1136/ard.41.2.168.
We studied the effect of human interstitial collagen types I, II, and III on serum-free cultured mouse macrophages and on the complement classical and alternative pathways in human and guinea-pig serum. Type II collagen produced a dose-dependent consumption and conversion of C3 and factor B both in the homologous and in the heterologous system. This effect on the alternative pathway was reproduced in genetically C4-deficient guinea-pig serum and could be triggered by native, triple helical type II molecules, by their component alpha chains, and the CNBr peptide mixture. Addition of type II collagen to the mouse macrophage cultures induced not only a dose- and time-dependent secretion of lysosomal enzymes, but also the generation of a supernatant factor cytotoxic for mouse mastocytoma P 815 cells. Collagen of types I and III were conspicuously less active or inactive in all assays. The studies demonstrate properties of the collagen specific for cartilage which, on a molecular level, suggest its direct, local participation in the production and perpetuation of rheumatoid arthritis.
我们研究了人I型、II型和III型间质胶原对无血清培养的小鼠巨噬细胞以及对人血清和豚鼠血清中补体经典途径和替代途径的影响。II型胶原在同源和异源系统中均产生剂量依赖性的C3和B因子消耗及转化。在遗传性C4缺陷的豚鼠血清中再现了对替代途径的这种作用，并且该作用可由天然的三螺旋II型分子、其组成的α链以及溴化氰肽混合物触发。向小鼠巨噬细胞培养物中添加II型胶原不仅诱导溶酶体酶的剂量和时间依赖性分泌，还诱导产生对小鼠肥大细胞瘤P 815细胞具有细胞毒性的上清因子。I型和III型胶原在所有测定中明显活性较低或无活性。这些研究证明了软骨特异性胶原的特性，在分子水平上表明其直接、局部参与类风湿性关节炎的产生和持续存在。
