HUMORAL AND CELLULAR IMMUNE-MECHANISMS OF NEUTROPENIA IN PATIENTS WITH FELTYS SYNDROME

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  • 1 January 1980
    • journal article
    • research article
    • Vol. 39  (2) , 307-314
Abstract
The objective of these studies was to assess the relative role of humoral or cellular immune mechanisms in the neutropenia of Felty''s syndrome. Amounts of neutrophil-bound Ig[immunoglobulin]G were measured by a sensitive antiglobulin inhibition assay. These values were increased in 8 of 17 patients with Felty''s syndrome over the highest values seen in 17 patients with rheumatoid arthritis without leukopenia or 26 normal individuals. Levels of serum IgG neutrophil-binding activity from 13 of 21 patients with Felty''s syndrome were greater than the highest values seen with normal sera compared to 6 of 30 sera from patients with rheumatoid arthritis alone. A strong correlation was observed between levels of direct neutrophil-bound IgG and serum IgG neutrophil-binding activity for the 17 patients with Felty''s syndrome. Inhibition of normal marrow granulocyte colony growth greater than 40% was seen with the peripheral blood mononuclear leukocytes from 5 of 11 patients with Felty''s syndrome. All 5 patients had normal levels of neutrophil bound IgG and normal to moderately increased levels of serum IgG neutrophil binding activity. Of the 6 patients whose mononuclear leukocytes did not inhibit granulocyte colony growth, 3 had markedly elevated levels of neutrophil-bound IgG and 4 had elevated levels of serum IgG neutrophil binding activity. Humoral and cellular immune mechanisms of neutropenia may be present in different subsets of patients with Felty''s syndrome.