Antigen(Ag)-immunoglobulin (Ig)G complexes (IC) are more efficiently processed and presented than soluble Ag. IC can bind to various cell types via different types of Fc-Receptors or, upon binding to complement factors, by complement receptors. Murine professional antigen-presenting cells (APC) express four types of FcgammaReceptors (FcgammaR) via which they are able to capture IC; three activating receptors (FcgammaRI, III and IV) and one inhibitory receptor (FcgammaRII). It has been demonstrated that FcgammaR play a pivotal role in facilitating the presentation of Ag derived from IC. Nonetheless, relative little information is available on the relative contribution of the activating or inhibitory FcgammaR or complement to the presentation of immune-complexed Ag to CD8+ T cells. To study the contribution of the different FcgammaR and complement receptors in IC-facilitated Ag-presentation, we analyzed the ovalbumin(OVA)-specific CD8+ T cell proliferation in FcgammaR- and complement component 3 (C3)-deficient mice after subcutaneous injection of OVA-IC. Here we show that the efficient Ag-presentation was FcgammaR-, but not C3-mediated, as it was inhibited in FcgammaRI/II/III-deficient mice but unaffected in the C3-depleted mice. Moreover, FcgammaRIV does not play a role under these conditions. However, no difference was found between wild-type and FcgammaRI/III-deficient or wild-type and FcgammaRII-deficient mice. These results indicate that Ag-presentation via the activating FcgammaR is not enhanced in the absence of FcgammaRII, and point to redundancy of the FcgammaR, including FcgammaRII, in the uptake and presentation of s.c. injected soluble IC to CD8+ T cells.