Doe W F, Henson P M
J Immunol. 1979 Nov;123(5):2304-10.
Peritoneal macrophages from the endotoxin-unresponsive C3H/HeJ substrain of mice were entirely refractory to activation in vitro by protein-free LPS, a defect that was not overcome by co-culture of spleen cells from the responder C3H/St substrain with LPS resistant C3H/HeJ macrophages. The defect in responsiveness appears confined to the lipid A activation signal since C3H/HeJ macrophages were fully activated after in vitro treatment by lipid A protein (LAP)--LPS complex, isolated LAP, and BCG. Moreover, after exposure to allogeneic tumor cells in vivo, C3H/HeJ macrophages were cytotoxic for tumor target cells in vitro. By contrast, macrophages from the responder C3H/St strain were fully activated by protein-free LPS to become cytolytic for tumor cells in vitro. C3H/HeJ macrophages, therefore, exhibit a highly selective defect characterized by unresponsiveness to the lipid A activation signal of protein-free LPS and resistance to the toxic effects of high concentrations of LPS that were lethal to the responder C3H/St strain.
来自内毒素无反应性小鼠品系C3H/HeJ的腹腔巨噬细胞在体外对无蛋白脂多糖（LPS）的激活完全具有抗性，将反应性C3H/St品系的脾细胞与LPS抗性C3H/HeJ巨噬细胞共培养也无法克服这一缺陷。反应性缺陷似乎仅限于脂质A激活信号，因为C3H/HeJ巨噬细胞在体外经脂质A蛋白（LAP）-LPS复合物、分离的LAP和卡介苗处理后被完全激活。此外，在体内暴露于同种异体肿瘤细胞后，C3H/HeJ巨噬细胞在体外对肿瘤靶细胞具有细胞毒性。相比之下，来自反应性C3H/St品系的巨噬细胞被无蛋白LPS完全激活，在体外对肿瘤细胞具有溶细胞作用。因此，C3H/HeJ巨噬细胞表现出高度选择性缺陷，其特征是对无蛋白LPS的脂质A激活信号无反应，并且对高浓度LPS的毒性作用具有抗性，而高浓度LPS对反应性C3H/St品系是致命的。
