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Nonspecific activation of complement by leukemic cells
Non-specific activation of complement (NAC) on cell membranes via the alternative pathway was studied by using leukemic cells and cells from a generalized reticulohistiocytosis. The cells were treated with normal human serum in veronal-buffered saline containing ethyleneglycoltetraacetrate and MG++. Since human erythrocytes (HuE) are known to adhere to complement-reacted cell membranes in an immune adherence reaction, complement activation on the cell membrane was confirmed by the rosette formation of HuE which is due to the generation of C3b molecules on the cell membrane. Only cells from Schilling-type acute monocytic leukemias and cells from a generalized reticulohistiocytosis possessed NAC ability. All other leukemic cells tested, as well as normal hematopoietic and lymphoreticular cells, were NAC-negative. Furthermore, none of the mitogens tested generated NAC ability on normal peripheral blood lymphocytes.
Non-specific activation of complement (NAC) on cell membranes via the alternative pathway was studied by using leukemic cells and cells from a generalized reticulohistiocytosis. The cells were treated with normal human serum in veronal-buffered saline containing ethyleneglycoltetraacetrate and MG++. Since human erythrocytes (HuE) are known to adhere to complement-reacted cell membranes in an immune adherence reaction, complement activation on the cell membrane was confirmed by the rosette formation of HuE which is due to the generation of C3b molecules on the cell membrane. Only cells from Schilling-type acute monocytic leukemias and cells from a generalized reticulohistiocytosis possessed NAC ability. All other leukemic cells tested, as well as normal hematopoietic and lymphoreticular cells, were NAC-negative. Furthermore, none of the mitogens tested generated NAC ability on normal peripheral blood lymphocytes.