Human monocytes released superoxide anion, prostaglandin E2, leukotriene B4, Il-1, and TNF when exposed to plastic surfaces coated with murine anti-CD3 monoclonal antibody, OKT3. Stimulation of mediator release by OKT3 was dependent on the amount of antibody immobilized onto wells of plastic tissue culture plates. Soluble antibody or antibody adsorbed to monocytes and reacted with an aggregating (""""""""cross-linking"""""""") second antibody failed to induce mediator release. Monocytes """"""""armed"""""""" with OKT3 formed rosettes with T cells in a fashion indistinguishable from that seen between monocytes and sensitized T cells. Monocytes with absorbed OKT3 antibodies released Il-1Beta and TNF-alpha when exposed to unsensitized T cells, although increased superoxide release could not be detected. OKT4a, a murine IgG2 antibody which reacts with a different T cell epitope (CD4), failed to induce cytokine release from monocytes when cross-linked by T cells or a CD4+ T cell line, even in the presence of IL-2 or IFN-gamma. These data indicate that certain antibodies bound to Fc receptors of monocytes may trigger monocyte function when reacting with cells bearing the appropriate target antigens. FcR-mediated signalling resulting in mediator release may be involved in initiating or regulating the immune response. Furthermore, systemically administered monoclonal antibodies may induce inflammatory responses and their attendant symptomatologies via their interaction with FcR-bearing inflammatory cells.
