Orr F W, Varani J, Kreutzer D L, Senior R M, Ward P A
Am J Pathol. 1979 Jan;94(1):75-83.
Leukocytes contain within their lysosomal granules enzymatic activity that will generate from C5 chemotactic activity for leukocytes (neutrophils) and tumor (Walker carcinosarcoma) cells. Similar activity has been found in phagocytic supernatant fluids from neutrophils and in purified preparations of the leukocyte neutral proteases elastase and cathepsin G. White leukotactic activities can be generated from either the third (C3) or the fifth (C5) components of complement, only C5 serves as a source for generation of the chemotactic activity for tumor cells. As has been previously shown with trypsin, the C5-related chemotactic activities generated by leukocyte proteases are time-dependent: leukotactic activity appears early, then disappears, and is replaced by chemotactic activity for tumor cells. The generation of these chemotactic activities from C5 is blocked by prior treatment of leukocyte preparations with the neutral protease inhibitor Trasylol. The demonstration that enzyme activities from leukocytes have the ability to generate tumor cell chemotactic factors from C5 suggests a possible mechanism by which the development of metastatic lesions may be promoted at sites of tissue injury or inflammation.
白细胞的溶酶体颗粒中含有酶活性,这种活性可从C5产生对白细胞(中性粒细胞)和肿瘤(沃克癌肉瘤)细胞的趋化活性。在中性粒细胞的吞噬上清液以及白细胞中性蛋白酶弹性蛋白酶和组织蛋白酶G的纯化制剂中也发现了类似的活性。白细胞趋化活性可由补体的第三(C3)或第五(C5)成分产生,但只有C5可作为肿瘤细胞趋化活性的来源。如先前用胰蛋白酶所显示的那样,白细胞蛋白酶产生的与C5相关的趋化活性是时间依赖性的:白细胞趋化活性先出现,然后消失,取而代之的是对肿瘤细胞的趋化活性。用中性蛋白酶抑制剂抑肽酶预先处理白细胞制剂可阻断这些来自C5的趋化活性的产生。白细胞的酶活性能够从C5产生肿瘤细胞趋化因子,这一证明提示了一种可能的机制,通过该机制,转移性病变的发展可能在组织损伤或炎症部位得到促进。