FcγRII restriction fragment length polymorphism (RFLP): analysis in systemic lupus erythematosus and scleroderma and evidence of an alpha gene duplication

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Abstract
SUMMARY: The characteristic finding of high levels of circulating immune complexes in patients with the autoimmune connective tissue diseases systemic lupus erythemalosus (SLE) or scleroderma has raised the possibility that these patients may have a primary defect in immune complex clearance. The Fc receptor for IgG (FcγR) plays a central role in the phagocytosis of antibody complexes. We have analysed FcγR (type II) RFLPs identified in TaqI-and MspI-restrictcdgenomic DNAand found that their distribution in SLE and selerodenna did not differ significantly from controls. Hybridization with specific regions of the FcγRII cDNA clone indicate that part of the FcγRIIα locus is duplicated in some individuals. A further FcγRII gene has recently been identified (FcγRIIα). This gene shows > 95% homology with FcγRIIα and may thus be the candidate gene for the apparant α duplication seen in some individuals. It is possible that an individual may possess one. two, three or four TaqI FcγRIIα/α′alleles. correlating with incidence and numerical heterogeneity in FcγRIIα and α′. The physiological effects of this numerical heterogeneity remain to be investigated.