Abstract
Raji, a human B lymphoblastoid cell line has the ability to activate the complement cascade by alternate pathway mechanisms with subsequent fixation of C3 to receptors on the Raji cell membrane. Using this property, we examined the role that complement plays in mediating a cytolytic event between human peripheral blood monocytes and Raji cells coated with C3b, antibody, or both. Presence of C3 was confirmed by immune adherence. IgG bound to the Raji membrane was quantitated using I 125 Staphylococcal protein A assay. The presence of alternate pathway-activated C3 on Raji cells failed to produce monocyte-mediated cytotoxicity. These same target cells subsequently coated with antibody concentration ranging from 200 to >600,000 SPA molecules per Raji cell produced neither enhancement nor inhibition of antibody-dependent, cell-mediated cytotoxicity (ADCC). ADCC was enhanced by complement when complement activation and binding of C3 to the cell surface occurred by classical pathway mechanisms. ADCC of 32% ± 3.2 occurred with undiluted antiserum (625,000 SPA molecules bound/Raji cell) with enhancement to 52% ± 1.1 in the presence of C3. IgG inhibition of ADCC was unaffected by the presence of membrane-bound C3.
Highlights
Peripheral blood monocytes are the precursors of tissue macrophages and possess membrane receptors for the Fc region of IgG immunoglobulin (Fc receptor) and the third component of complement (C3) [1]
Raji cells coated with C3 alone via alternate pathway activation [14, 15] were prepared by incubation of 3 x lo6 cells with 60 ~1 of normal fresh serum or Cd-deficient serum for 20 min at 37°C
A third target were Raji cells coated with C3 by alternate pathway activation and coated with antibody by incubation with rabbit immune sera
Summary
Peripheral blood monocytes are the precursors of tissue macrophages and possess membrane receptors for the Fc region of IgG immunoglobulin (Fc receptor) and the third component of complement (C3) [1]. The Fc receptor allows these cells to interact with antibody-coated red cells [2] and tumor cells [3] resulting in target cell damage and lysis. This reaction has been termed antibody-dependent, cellular cytotoxicity (ADCC) and several cell types which bear membrane Fc receptors can act as effector cells, i.e., granulocytes [4], monocytes [5], and K lymphocytes [6,7]. Kurlander has examined the interaction of blood monocytes with red cell targets coated with IgG immunoglobulin and/or C3 [13] They concluded that C3 on the target cell surface can enhance ADCC but not mediate cytolysis directly. This B-cell lymphoblast cell line was chosen because it is capable of activating the alternate complement pathway resulting in C3-coated tumor cells independent of antibody [14, 15]
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