FcγRII/CD32-negative human Langerhans cells may be responsible for the immunostimulatory activity of freshly isolated epidermal cells

Abstract

Cultured murine and human epidermal Langerhans cells (LC) undergo a phenotypical and functional maturation process. In fact, they loose FcγRII and Birbeck granules, increase HLADR expression, and become potent accessory cells for allogeneic MLR. However, resident/freshly isolated human epidermal LC represent a phenotypically heterogeneous cell population. Indeed, a subset of CD1a + LC lacks Birbeck granules, is FcγRII/CD32 −, and strongly expresses HLADR and the RFD1 antigen that is considered to be specific for interdigitating cells. In the present study the functional capacity of this FcγRII/CD32 − CD1a + LC subset was investigated in MLR assays by comparing the stimulatory activity of freshly isolated crude epidermal cells (EC) with that of freshly isolated EC depleted in CD1a + or in FcγRII + cells. Thereby, we observed that crude EC stimulated allogeneic PBMC while the removal of CD1a + cells abrogated this stimulation. However, crude EC depleted in FcγRII/CD32 + cells still exhibited a stimulatory capacity that was at least equal to that of crude EC. Taken together, these data suggest that among resident human epidermal LC there exists a subset of phenotypically and functionally more differentiated cells that may be solely responsible for the stimulatory capacity of freshly isolated crude EC.