Ito M, Watanabe M, Kamiya H, Sakurai M
Department of Pediatrics, Mie University School of Medicine, Japan.
Viral Immunol. 1996;9(4):219-24. doi: 10.1089/vim.1996.9.219.
We investigated the roles of CD11a, CD11b, CD18, and CD54 adhesion molecules in non-adherent peripheral blood mononuclear cells (NPBMC)-induced DNA fragmentation of cytomegalovirus (CMV)-infected cells. DNA fragmentation in the supernatant from CMV-infected cells and NPBMC was assayed, and cytotoxicity against CMV-infected cells was calculated. Treatment of NPBMC with monoclonal antibodies to CD11a, CD11b, CD18, and CD54 significantly reduced cytotoxicity against CMV-infected cells. A combination of anti-CD11a, anti-CD11b, and anti-CD18 antibodies further inhibited cytotoxicity against CMV-infected cells. Cytotoxicity against CMV-infected cells treated with anti-CD54 antibody was also significantly inhibited. Binding of effector cells to target cells was not affected by treatment of NPBMC or CMV-infected cells with antiadhesion molecule antibodies. These results indicate that LFA-1 (CD11a/CD18), Mac-1 (CD11b/CD18), and ICAM-1 (CD54) adhesion molecules are involved in natural killer (NK) cell-induced DNA fragmentation in CMV-infected cells.
我们研究了CD11a、CD11b、CD18和CD54黏附分子在非黏附性外周血单个核细胞（NPBMC）诱导的巨细胞病毒（CMV）感染细胞DNA片段化中的作用。检测了CMV感染细胞和NPBMC上清液中的DNA片段化情况，并计算了对CMV感染细胞的细胞毒性。用抗CD11a、CD11b、CD18和CD54单克隆抗体处理NPBMC可显著降低对CMV感染细胞的细胞毒性。抗CD11a、抗CD11b和抗CD18抗体联合使用可进一步抑制对CMV感染细胞的细胞毒性。抗CD54抗体处理的CMV感染细胞的细胞毒性也受到显著抑制。用抗黏附分子抗体处理NPBMC或CMV感染细胞并不影响效应细胞与靶细胞的结合。这些结果表明，淋巴细胞功能相关抗原-1（LFA-1，CD11a/CD18）、巨噬细胞-1抗原（Mac-1，CD11b/CD18）和细胞间黏附分子-1（ICAM-1，CD54）黏附分子参与了自然杀伤（NK）细胞诱导的CMV感染细胞DNA片段化过程。
