The objective of these studies was to assess the relative role of humoral or cellular immune mechanisms in the neutropenia of Feltry's syndrome. The amounts of neutrophil-bound IgG were measured by a sensitive antiglobulin inhibition assay. These values were increased in eight out of seventeen patients with Felty's syndrome over the highest values seen with seventeen patients with rheumatoid arthritis without leukopenia or twenty-six normal individuals. The levels of serum IgG neutrophil-binding activity from thirteen out of twenty-one patients with Felty's syndrome were greater than the highest values seen with normal sera compared to six out of thirty sera from patients with rheumatoid arthritis alone. A strong correlation was observed between the levels of direct neutrophil-bound IgG and the serum IgG neutrophil-binding activity for the seventeen patients with Felty's syndrome. Inhibition of normal marrow granulocyte colony growth greater than 40% was seen with the peripheral blood mononuclear leucocytes from five out of eleven patients with Feltry's syndrome. All five patients had normal levels of neutrophil bound IgG and normal to moderately increased levels of serum IgG neutrophil binding activity. In contrast, of the six patients whose mononuclear leucocytes did not inhibit granulocyte colony growth, three had markedly elevated levels of neutrophil-bound IgG and four had elevated levels of serum IgG neutrophil binding activity. These results suggest that humoral and cellular immune mechanisms of neutropenia may be present in different subsets of patients with Felty's syndrome.