Shiku H, Takahashi T, Bean M A, Hämmerling U, Oettgen H F, Old L J
Isr J Med Sci. 1976 Apr-May;12(4-5):425-34.
The participation of B cells in cell-mediated cytotoxicity (CMC) for allogeneic and syngeneic murine sarcoma cells induced with 3-methylcholanthrene was investigated. Primed nonadherent peritoneal cells (NAPC) were treated with antisera against lymphocyte surface antigens and complement, and residual CMC activity was measured with the [3H]proline microassay. The antisera (anti-PC.1 and various anti-Ig sera) used for this purpose were highly reactive with B cells according to established serologic criteria. Elimination of cells that carried PC.1 or Ig on their surface did not diminish CMC of NAPC for allogeneic or syngeneic tumor cells. Exposure of cytotoxic NAPC to various anti-Ig antisera (without complement) before and during the CMC assay did not inhibit CMC either. We conclude that under these conditions CMC is not mediated by B cells, nor is it dependent on their presence. In addition, our findings do not implicate any of the usual classes and types of Ig covered by the Ig antisera used in this study as constituting specific receptors on the effector T cells of CMC.
研究了B细胞在由3 - 甲基胆蒽诱导的同种异体和同基因小鼠肉瘤细胞的细胞介导细胞毒性(CMC)中的参与情况。用抗淋巴细胞表面抗原的抗血清和补体处理致敏的非贴壁腹膜细胞(NAPC),并通过[³H]脯氨酸微量测定法测量残余的CMC活性。根据既定的血清学标准,用于此目的的抗血清(抗PC.1和各种抗Ig血清)与B细胞具有高度反应性。消除表面携带PC.1或Ig的细胞并没有降低NAPC对同种异体或同基因肿瘤细胞的CMC。在CMC测定之前和期间,将细胞毒性NAPC暴露于各种抗Ig抗血清(无补体)也不会抑制CMC。我们得出结论,在这些条件下,CMC不是由B细胞介导的,也不依赖于它们的存在。此外,我们的研究结果并未表明本研究中使用的Ig抗血清所涵盖的任何常见Ig类别和类型构成CMC效应T细胞上的特异性受体。