Mehta K, Claringbold P, Lopez-Berestein G
J Immunol. 1987 Jun 1;138(11):3902-6.
Mouse resident peritoneal macrophages, activated in vitro with murine recombinant interferon-gamma and lipopolysaccharide in the presence of sera from different sources, showed marked differences in their abilities to inhibit murine adenocarcinoma cell growth, and in induced activity of the enzyme, tissue transglutaminase. The extraction of lipids from the serum abolished its ability to induce tissue TGase activity and to inhibit cytostatic activity, but these capabilities were fully restored by readdition of all trans-retinol or all trans-retinoic acid at physiological concentrations. Addition of dansylcadaverine, a competitive inhibitor of TGase, resulted in complete recovery of macrophages from retinoid-induced suppression of cytostatic activity. These results suggest that endogenous retinoids play an important role in the regulation of macrophage-mediated cytostatic activity in a process that is independent of prostaglandin secretion but seems to involve the protein cross-linking enzyme, tissue transglutaminase.
在来自不同来源血清存在的情况下，用小鼠重组干扰素-γ和脂多糖在体外激活的小鼠腹腔常驻巨噬细胞，在抑制小鼠腺癌细胞生长的能力以及诱导组织转谷氨酰胺酶的活性方面表现出显著差异。从血清中提取脂质消除了其诱导组织转谷氨酰胺酶活性和抑制细胞生长抑制活性的能力，但通过重新添加生理浓度的全反式视黄醇或全反式视黄酸，这些能力得以完全恢复。添加转谷氨酰胺酶的竞争性抑制剂丹磺酰尸胺，可使巨噬细胞从类视黄醇诱导的细胞生长抑制活性抑制中完全恢复。这些结果表明，内源性类视黄醇在调节巨噬细胞介导的细胞生长抑制活性过程中发挥重要作用，该过程独立于前列腺素分泌，但似乎涉及蛋白质交联酶——组织转谷氨酰胺酶。
