Appearance in trypsinized normal cells of reactivity with antibody presumably specific for malignant cells.

Abstract

Trypsinization of normal human diploid cells (WI-38 and MRC 5) resulted in the appearance of complement-fixing reactivity with an immunoglobulin (anti-HeLa G globulin), prepared against a purified HeLa (malignant human) cell antigen (G), which reacts with various malignant human cell lines and tumors but not with certain normal human cells. The presence of receptors in the nonreacting, untrypsinized normal human cells and the specificity of the reactive groups that appeared after trypsinization was established by the fact that the antibody could be completely absorbed with large quantities of packed, untrypsinized human cells but not with similar quantities of either rabbit or guinea-pig kidney tissue-culture cells, which did not react with this antibody either before or after treatment with trypsin. The change produced by trypsinization is thus similar to the previously demonstrated appearance of reactive groups with the same anti-HeLa G globulin in normal human cells at certain times after infection with herpes simplex and vaccinia viruses. The fact that the trypsinized WI-38 cells absorbed more antibody than the same number of cells before trypsinization indicated that trypsinization resulted not only in the appearance of reactivity with antibody but also in a greater concentration of combining receptors, which is unlike the situation with lectins producing agglutinability without an increase in the number of receptors. Moreover, the fact that absorption with trypsinized normal cells removed larger amounts not only of the antibody reacting with the trypsin-treated WI-38 cells but also of antibody that reacts with WI-38 cells infected with herpes simplex virus and with the malignant HEp-2 cells, suggests that the combining groups that emerge after trypsinization of the normal human cells are the same or similar to those present in malignant human cells (HEp 2) and to those that emerge after infection of the normal human cells with herpes simplex virus.