We have shown that mycoplasmas bind spontaneously to neutrophils, as well as directly activating the first component of complement with probable subsequent binding through neutrophil complement receptors. Thus, antibody is not required to opsonize mycoplasmas for neutrophil phagocytosis. Furthermore, mycoplasmas remain viable when phagocytosed in the absence of antibody and may be carried inside neutrophils to various parts of the body to cause infection (e.g. joints). We found that antibody alone inhibits the growth of mycoplasmas in vitro. These observations suggest that the role of antibodies is to control the growth of mycoplasmas on mucosal surfaces; neutrophils play no part in defence and may even aid dissemination of the infection. This helps to explain why patients with hypogammaglobulinaemia are prone to systemic mycoplasma infections.