Complement-derived peptides capable of activating neutrophils appear in plasma during flares of systemic lupus erythematosus (SLE). One possible consequence of such activation is an increased expression of the surface adhesion promoting heterodimer gp165/95 (the complement receptor CR3). The quantity of gp165/95 was measured by indirect immunofluorescence using a monoclonal antibody of the CD11b group. Mol, directed to the alpha chain. Eighty-three percent of 26 patients with SLE expressed gp165/95 on their neutrophil surface to a greater extent than normals. The highest levels of surface gp165/95 were found in patients with the most severe disease, who also had the highest levels of the circulating anaphylatoxin C3a (mean = 560 ng/ml versus 147 ng/ml in controls). There was a negative correlation between expression of gp165/95 and absolute neutrophil count. Five individuals followed serially demonstrated an increase in surface gp165/95 during disease flares which returned to normal with clinical improvement. These data support the hypothesis that the neutrophils of patients with active SLE recruit increased numbers of gp165/95 molecules to their surface in respose to complement activation; these activated neutrophils bearing increased numbers of adhesion promoting gp165/95 may contribute to endothelial injury in SLE.