Antibody-dependent cellular cytotoxicity of Coxiella burnetii-infected J774 macrophage target cells.

Cell-mediated immunity is clearly the critical host defense mechanism against human Coxiella burnetii infection (Q fever); the role of specific antibody is unclear. By using a mouse macrophage tumor cell line, J774, persistently infected with C. burnetii phase I organisms, in a standard 51Cr-release cytotoxicity assay, we explored the possibility that antibody-dependent cellular cytotoxicity may be immune mechanism in Q fever. After 16 h of incubation in the presence of immune sera from Q fever hepatitis or endocarditis patients, nonimmune human peripheral blood effector cells specifically lysed infected J774 target cells; no 51Cr release was seen in the presence of nonimmune sera or uninfected target cells. An effector/target ratio of at least 5:1 was required, and monocytes were more efficient effector cells than lymphocytes. Cytotoxicity was blocked by preincubation of effector cells with purified aggregated human immunoglobulin G, indicating the role of Fc receptor-bearing effector cells. Two nonphagocytic lymphoid tumor cell targets, passively coated with C. burnetii, did not induce substantial immune-specific cytolysis, suggesting that bystander lysis does not explain the observation of specific lysis. Although antibody-dependent cellular cytotoxicity may participate in primary defense, alternatively, it may facilitate the dissemination of C. burnetii or surreptitiously participate in granuloma formation.