• 1 January 1977
    • journal article
    • research article
    • Vol. 27  (2) , 285-291
Abstract
Direct labeling of cell surface protein with 125I has enabled measurements to be made of lymphocyte membrane turnover. In CLL cells this is evidently much retarded in comparison with normal lymphocytes, and slow replacement of cell surface proteins might be responsible for lack of membrane mobility and poor immunological responses. Serum from CLL patients enhanced viability of the leukemic cells in culture and the interaction of these serum factors with the CLL cell membrane gives rise to rapid replacement of surface proteins. Thus the rate of membrane turnover in vivo would be comparable with that of normal lymphocytes. Lack of cell-surface mobility and poor membrane biosynthesis can not be held responsible for poor immunological activity in vivo. Autoimmune antibodies binding to the surface of CLL cells may spatially inhibit activation by ligands.