Dermal microvascular endothelial cells express CD32 receptors in vivo and in vitro

Abstract

Immune complexes are thought to be the major cause of cutaneous necrotizing vasculitis, but the mechanism of immune complex targeting to specific vessels is largely unknown. In myelomonocytic cells, immune complex binding and receptor-mediated endocytosis are mediated by Fc γ R. We asked whether dermal microvascular endothelial cells (DMEC) express Fc γ Rs. In cryostat sections of normal human skin, mAb IV.3 or AT10, both recognizing CD32 (Fc γ RII), localizes to the luminal surface of DMEC of the superficial but not of the deep vascular plexus. All DMEC do not express CD16 (Fc γ RIII) or CD64 (Fc γ RI) molecules. Adult skin-derived DMEC in culture express CD32 (Fc γ RII) molecules, as measured by FACS, but are negative for CD16 or CD64. HUVEC, tested for comparison, do not express CD16, 32, or 64 proteins. By reverse-transcriptase PCR and subsequent Southern blot analysis, the isoform of the CD32 molecule expressed on DMEC is determined as Fc γ RIIa. HUVEC do not contain Fc γ RIIa or Fc γ RIIb mRNA. In DMEC, Fc γ RIIa cross-linking results in immediate intracellular free Ca2+ ([Ca2+]i) concentration fluxes and in rapid internalization of the occupied receptors. We conclude that DMEC are equipped with fully functional Fc γ RIIa molecules.