Hahne M, Rimoldi D, Schröter M, Romero P, Schreier M, French L E, Schneider P, Bornand T, Fontana A, Lienard D, Cerottini J, Tschopp J
Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland.
Science. 1996 Nov 22;274(5291):1363-6. doi: 10.1126/science.274.5291.1363.
Malignant melanoma accounts for most of the increasing mortality from skin cancer. Melanoma cells were found to express Fas (also called Apo-1 or CD95) ligand (FasL). In metastatic lesions, Fas-expressing T cell infiltrates were proximal to FasL+ tumor cells. In vitro, apoptosis of Fas-sensitive target cells occurred upon incubation with melanoma tumor cells; and in vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation. In contrast, tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL. Thus, FasL may contribute to the immune privilege of tumors.
恶性黑色素瘤是皮肤癌死亡率上升的主要原因。研究发现黑色素瘤细胞表达Fas（也称为Apo-1或CD95）配体（FasL）。在转移性病变中，表达Fas的T细胞浸润靠近FasL+肿瘤细胞。在体外，Fas敏感靶细胞与黑色素瘤肿瘤细胞孵育后发生凋亡；在体内，向小鼠注射FasL+小鼠黑色素瘤细胞会导致肿瘤迅速形成。相比之下，在Fas缺陷的lpr突变小鼠中，免疫效应细胞不能被FasL杀死，肿瘤发生延迟。因此，FasL可能有助于肿瘤的免疫逃逸。
