Halliday G M, Dickinson J L, Muller H K
Department of Pathology, University of Tasmania, Hobart, Australia.
Immunology. 1989 Jul;67(3):298-302.
Retinoic acid prevents the decrease in epidermal Langerhans' cell (LC) density which occurs upon application of the tumour promotor 12-O-tetradecanoylphorbol 13-acetate (TPA) to murine skin. This occurred very rapidly, after only 1 week, and was still observed after 4 weeks of treatment. Retinoic acid alone increased the LC density, indicating that it could affect LC density independently of TPA. The induction of a contact sensitivity response which was inhibited by prior treatment with TPA due to the low LC density was also protected by retinoic acid. The anti-carcinogenic activity of retinoic acid is partially the result of its ability to inhibit tumour promotion. The loss of LC may be one of the important steps in tumour promotion as this would allow developing tumours to escape immune destruction. Our studies suggest that the ability of retinoic acid to suppress tumour promotion may be in part by protecting local antigen-presenting cells, thus allowing an immune response to be generated against tumours.
视黄酸可防止在将肿瘤促进剂12-O-十四烷酰佛波醇-13-乙酸酯(TPA)应用于小鼠皮肤后发生的表皮朗格汉斯细胞(LC)密度降低。这种情况在仅1周后就非常迅速地发生了,并且在治疗4周后仍可观察到。单独使用视黄酸可增加LC密度,表明它可独立于TPA影响LC密度。由于LC密度低而被TPA预处理抑制的接触敏感性反应的诱导也受到视黄酸的保护。视黄酸的抗癌活性部分是其抑制肿瘤促进能力的结果。LC的丧失可能是肿瘤促进的重要步骤之一,因为这将使正在发展的肿瘤逃避免疫破坏。我们的研究表明,视黄酸抑制肿瘤促进的能力可能部分是通过保护局部抗原呈递细胞,从而允许产生针对肿瘤的免疫反应。