Murine plasmacytoid dendritic cells express the inhibitory FcγRIIB as their sole FcγR and fail to mediate antigen presentation of immune complexes to T cells

Abstract

Plasmacytoid DC's (pDCs) in their role as Type I IFN producers, are key regulators of the innate immune response, yet their role in the adaptive immune response remains unclear. The ability of murine pDCs to present antigen in immune complexes (ICs) to T cells was examined. Unlike conventional DCs, ovalbumin‐IC exposed murine pDCs failed both to upregulate costimulatory molecules and to activate OVA specific CD4+ and CD8+ T cells. The failure of murine pDCs to promote T cell activation through either the exogenous or cross‐presentation pathways occurred despite IC binding and internalization. ICs internalized by pDCs however were inefficiently delivered to an intracellular degradative compartment. This defect in the IC processing capability is likely the consequence of a lack of activating Fc Receptor expression (FcRI, III, IV) and the exclusive expression of the inhibitory receptor FcRIIB. This selective expression of FcRIIB by pDCs was not strain dependent and was maintained even following stimulation with TLR ligands and inflammatory cytokines. Thus, pDCs are unable to effectively process ICs for antigen presentation, and may not be able to directly activate naive T cells in vivo.