Evaluation of the role of Fcγ and complement receptors in the decreased phagocytosis of hereditary haemochromatosis patients

Abstract

Hereditary haemochromatosis (HH) monocytes have a decreased antibody mediated phagocytosis of rabbit erythrocytes and Staphylococcus aureus compared to control monocytes. In order to investigate whether this decrease could be attributed to a different level of expression of Fcγ receptors (FcγR) or complement receptors (CR), which cooperate even in the absence of complement, the surface expression of these receptors was determined on monocyte-enriched suspensions. In contrast to what was expected, HH monocytes displayed a significantly higher level of FcγRI and FcγRIIa as compared to healthy donor monocytes, but these differences were very small. The expression of the other receptors studied were similar for both groups. The heat-inactivated mouse serum used for opsonizing the erythrocytes mainly contained mouse IgG1. Two genetically different forms of FcγRIIa are known, each with a different affinity for mouse IgG1 antibodies. Therefore, the FcγRIIa polymorphism in monocytes (MN) of both groups was also investigated. A similar distribution was found for patients and healthy donors. In addition, the extent of erythrophagocytosis of both donors and patients was independent of FcγRIIa allotype. Our results indicate that the altered phagocytosis by HH monocytes cannot be attributed to a different level of expression of receptors involved in phagocytosis or to FcγRIIa polymorphism.