Naganuma H, Kiessling R, Patarroyo M, Hansson M, Handgretinger R, Grönberg A
Department of Immunology, Karolinska Institute, Stockholm, Sweden.
Int J Cancer. 1991 Feb 20;47(4):527-32. doi: 10.1002/ijc.2910470410.
We have investigated the effect of interferon-gamma (IFN-gamma) treatment of neuroblastoma cells on the susceptibility to lysis by lymphokine-activated killer (LAK) cells and examined the participation of cell-adhesion molecules on the target cells in LAK cell lysis. Untreated neuroblastoma cells expressed lymphocyte-function-associated antigen 3 (LFA-3) and neural-cell-adhesion molecule (NCAM), but did not express MHC-class-I, MHC-class-II, or intercellular-adhesion molecule I (ICAM-I). IFN-gamma treatment of neuroblastoma cells induced the expression of MHC-class-I and ICAM-I antigens, but did not affect the expression of MHC-class-II, LFA-3, and NCAM. This was accompanied by an increased susceptibility to lysis by LAK cells. Anti-ICAM-I antibody inhibited partially the increased sensitivity of IFN-gamma-treated neuroblastoma cells to LAK cell lysis, and blocked completely the increase in binding of LAK cells observed after IFN-gamma treatment of the target cells. These results suggest that the increased LAK sensitivity of IFN-gamma-treated neuroblastoma cells is partially attributable to the induction of ICAM-I on neuroblastoma cells and indicate that post-binding events also play a role in the increased sensitivity to LAK cell lysis observed after IFN-gamma treatment.
我们研究了用γ-干扰素（IFN-γ）处理神经母细胞瘤细胞对其被淋巴因子激活的杀伤细胞（LAK细胞）裂解敏感性的影响，并检测了靶细胞上细胞黏附分子在LAK细胞裂解过程中的作用。未经处理的神经母细胞瘤细胞表达淋巴细胞功能相关抗原3（LFA-3）和神经细胞黏附分子（NCAM），但不表达MHC-Ⅰ类、MHC-Ⅱ类或细胞间黏附分子1（ICAM-Ⅰ）。用IFN-γ处理神经母细胞瘤细胞可诱导MHC-Ⅰ类和ICAM-Ⅰ抗原的表达，但不影响MHC-Ⅱ类、LFA-3和NCAM的表达。这伴随着对LAK细胞裂解敏感性的增加。抗ICAM-Ⅰ抗体部分抑制了经IFN-γ处理的神经母细胞瘤细胞对LAK细胞裂解敏感性的增加，并完全阻断了靶细胞经IFN-γ处理后观察到的LAK细胞结合增加。这些结果表明，经IFN-γ处理的神经母细胞瘤细胞对LAK敏感性的增加部分归因于神经母细胞瘤细胞上ICAM-Ⅰ的诱导，并表明结合后事件在经IFN-γ处理后观察到的对LAK细胞裂解敏感性增加中也起作用。
