In many cases, evidently inert and nontoxic biomaterials may trigger procoagulant and inflammatory responses. Because most polymeric biomaterials accumulate a surface layer of protein immediately after implantation, these adverse reactions may stem from secondary interactions between the host and this surface layer of adsorbed proteins. Using polyester terephthalate (the polymer from which both Dacron and Mylar are produced) as a model, we have explored the hypothesis that surface-adsorbed immunoglobulin might mediate subsequent inflammatory responses. We find, as have others, that immunoglobulin G (IgG) does spontaneously adsorb to polymer surfaces, both in vitro and in vivo. Furthermore, polymer implants precoated with IgG do activate human polymorphonuclear neutrophils in vitro and also attract substantial numbers of phagocytes (especially polymorphonuclear neutrophils and macrophages) when implanted in mice. However, when implants are placed in mice having a form of severe combined immunodeficiency (and, consequently, almost undetectable levels of serum IgG), a near-normal influx of phagocytic cells ensues. Thus, spontaneously-adsorbed surface IgG does not appear to be a necessary precedent to inflammatory responses directed against implanted biomaterials.