Johnson R L, Ziff M
J Clin Invest. 1976 Jul;58(1):240-52. doi: 10.1172/JCI108455.
Lymphokine-rich supernates from normal human peripheral blood mononuclear cells, stimulated by the mitogen phytohemagglutinin, have been shown to cause enhanced collagen accumulation by human embryonic lung fibroblasts (WI-38), as measured by hydroxyproline content of fibroblast monolayers, [14C] proline incorporation into soluble collagen and collagenase release of radioactivity in supernates and monolayers of cultures incubated with [14C] proline. This fibroblast-stimulating activity, demonstrable by suitable dilutions of the supernates, coexisted with a number of other lymphokine activities such as lymphotoxin, proliferation inhibitory factor, and cloning inhibitory factor, which tend to reduce the numbers of function of fibroblasts. The increased content of collagen appeared to be the product of selected surviving and responding fibroblasts. The factor causing this increased collagen accumulation was nondialyzable and stable at -70 degrees C. It represents the first described lymphoid cell-derived activity capable of enhancing collagen accumulation. Fibroblast-stimulating activity may be implicated in the abnormal fibrosis seen in association with chronic inflammation in a variety of disease states. It may have special relevance to progressive systemic sclerosis.
由促有丝分裂剂植物血凝素刺激正常人类外周血单个核细胞产生的富含淋巴因子的上清液，已被证明可导致人胚肺成纤维细胞（WI-38）的胶原积累增强，这是通过成纤维细胞单层的羟脯氨酸含量、[14C]脯氨酸掺入可溶性胶原以及在与[14C]脯氨酸一起培养的上清液和单层培养物中胶原酶释放的放射性来测量的。这种成纤维细胞刺激活性可通过上清液的适当稀释来证明，它与许多其他淋巴因子活性共存，如淋巴毒素、增殖抑制因子和克隆抑制因子，这些因子往往会减少成纤维细胞的数量或功能。胶原含量的增加似乎是选定的存活和反应性成纤维细胞的产物。导致这种胶原积累增加的因子不可透析，在-70℃下稳定。它代表了首次描述的能够增强胶原积累的淋巴细胞衍生活性。成纤维细胞刺激活性可能与多种疾病状态下与慢性炎症相关的异常纤维化有关。它可能与进行性系统性硬化症特别相关。
