DERMAL MICROVASCULAR ENDOTHELIAL-CELLS EXPRESS CD32 RECEPTORS IN-VIVOAND IN-VITRO

Immune complexes are thought to be the major cause of cutaneous necrot izing vasculitis, but the mechanism of immune complex targeting to spe cific vessels is largely unknown. In myelomonocytic cells, immune comp lex binding and receptor-mediated endocytosis are mediated by Fc gamma R. We asked whether dermal microvascular endothelial cells (DMEC) exp ress Fc gamma Rs. In cryostat sections of normal human skin, mAb IV.3 or AT10, both recognizing CD32 (Fc gamma RII), localizes to the lumina l surface of DMEC of the superficial but not of the deep vascular plex us. All DMEC do not express CD16 (Fc gamma RIII) or CD64 (Fc gamma RI) molecules. Adult skin-derived DMEC in culture express CD32 (Fc gamma RII) molecules, as measured by FAGS, but are negative for CD16 or CD64 . HUVEC, tested for comparison, do not express CD16, 32, or 64 protein s. Ey reverse-transcriptase PCR and subsequent Southern blot analysis, the isoform of the CD32 molecule expressed on DMEC is determined as F c gamma RIIa. HUVEC do not contain Fc gamma RIIa or Fc gamma RIIb mRNA . In DMEC, Fc gamma RIIa cross-linking results in immediate intracellu lar free Ca2+ ([Ca2+](i)) concentration fluxes and in rapid internaliz ation of the occupied receptors. We conclude that DMEC are equipped wi th fully functional Fc gamma RIIa molecules.