Gormus B J, Woodson M, Kaplan M E
Clin Exp Immunol. 1978 Nov;34(2):274-80.
Human peripheral blood lymphocytes (PBL) were incubated (stripped) with pronase or papain and compared with unstripped lymphocytes for their ability to mediate antibody-dependent, cell-mediated cytotoxicity (ADCC). Despite marked removal or inactivation of receptors for heat-aggregated IgG (aggG) by proteolytic digestion, and pronounced changes in the percentages of cells rosetting with IgG-sensitized erythrocytes (EA) (decreased by papain, increased by pronase), stripped PBL functioned normally in ADCC. Stripped and unstripped lymphocytes were pre-treated with aggG to determine the role of aggG receptors in ADCC. AggG almost totally abolished ADCC by unstripped PBL, but inhibited ADCC by enzyme-stripped lymphocytes relatively poorly. Neither untreated nor stripped PBL were able to induce cytotoxicity of chicken erythrocyte (CRBC) target cells sensitized with the Fab' fragment of anti-CRBC IgG antibody (CRBC-A). Exposure of PBL to EA monolayers composed of CRBC-A or of sheep erythrocytes (SRBC) sensitized with rabbit anti-SRBC IgG antibody (SRBC-A) depleted PBL of cells that rosetted with CRBC-A and with human Rh-positive, type O erythrocytes sensitized with the human anti-Rh serum Ripley (HRBC-A Ripley). Non-adherent cells were incapable of binding aggG and had markedly diminished cytotoxicity in ADCC. Similarly, exposure of PBL to HRBC-A Ripley monolayers resulted in non-adherent cells that were incapable of rosette formation with HRBC-A or CRBC-A, failed to bind aggG, and exhibited significantly diminished ADCC activity. These studies indicated that: (1) cytotoxic effector PBL active in ADCC (K cells) have receptors for aggG and for EA; (2) PBL deficient in functional aggG receptors (enzymatically inactivated or removed) are capable of inducing normal levels of ADCC; (3) aggG and EA receptors appear to be closely associated on native K-cell membranes; (4) there is no clear-cut relationship in a given lymphocyte population between the presence of either aggG or EA receptors and ADCC activity; and (5) populations of PBL binding HRBC-A Ripley overlap with, and may be identical to, those binding aggG and other types of EA complexes.
将人外周血淋巴细胞（PBL）用链霉蛋白酶或木瓜蛋白酶进行孵育（去除表面成分），并与未处理的淋巴细胞比较其介导抗体依赖性细胞介导的细胞毒性（ADCC）的能力。尽管通过蛋白水解消化显著去除或灭活了热聚集IgG（aggG）的受体，并且与IgG致敏红细胞（EA）形成花环的细胞百分比发生了明显变化（木瓜蛋白酶处理使其降低，链霉蛋白酶处理使其增加），但去除表面成分的PBL在ADCC中仍能正常发挥功能。将去除表面成分和未处理的淋巴细胞用aggG进行预处理，以确定aggG受体在ADCC中的作用。aggG几乎完全消除了未处理的PBL的ADCC作用，但对酶处理去除表面成分的淋巴细胞的ADCC作用抑制相对较弱。未处理的和去除表面成分的PBL均不能诱导用抗鸡红细胞IgG抗体（CRBC-A）的Fab'片段致敏的鸡红细胞（CRBC）靶细胞的细胞毒性。将PBL暴露于由CRBC-A或用兔抗绵羊红细胞IgG抗体（SRBC-A）致敏的绵羊红细胞（SRBC）组成的EA单层，可使与CRBC-A以及与人抗Rh血清里普利（HRBC-A Ripley）致敏的人Rh阳性O型红细胞形成花环的PBL细胞减少。非贴壁细胞不能结合aggG，并且在ADCC中的细胞毒性明显降低。同样，将PBL暴露于HRBC-A Ripley单层会产生非贴壁细胞，这些细胞不能与HRBC-A或CRBC-A形成花环，不能结合aggG，并且ADCC活性显著降低。这些研究表明：（1）在ADCC中具有活性的细胞毒性效应PBL（K细胞）具有aggG和EA的受体；（2）功能性aggG受体缺陷（酶促失活或去除）的PBL能够诱导正常水平的ADCC；（3）aggG和EA受体似乎在天然K细胞膜上紧密相关；（4）在给定的淋巴细胞群体中，aggG或EA受体的存在与ADCC活性之间没有明确的关系；（5）结合HRBC-A Ripley的PBL群体与结合aggG和其他类型EA复合物的群体重叠，并且可能相同。
