FcγRI (CD64) Contributes Substantially to Severity of Arthritis, Hypersensitivity Responses, and Protection from Bacterial Infection
- Ioan-Facsinay, A
- de Kimpe, S.J
- Hellwig, S.M.M
- van Lent, P.L
- Hofhuis, F.M.A
- van Ojik, H.H
- Sedlik, C
- da Silveira, S.A
- Gerber, J
- de Jong, Y.F
- Roozendaal, R
- Aarden, L.A
- van den Berg, W.B
- Saito, T
- Mosser, D
- Amigorena, S
- Izui, S
- van Ommen, G-J.B
- van Vugt, M
- van de Winkel, J.G.J
- Verbeek, J.S
DOIAbstract
AbstractThe high-affinity receptor for IgG, FcγRI, shares its capacity to bind IgG2a immune complexes (IgG2a-IC) with the low-affinity receptor FcγRIII and complement factors, hampering the definition of its biological role. Moreover, in vivo, FcγRI is occupied by monomeric IgG2a, reducing its accessibility to newly formed IgG2a-IC. By using a variety of FcγR−/− mice, we demonstrate that in the absence of FcγRI, the IgG2a-IC-induced cellular processes of phagocytosis, cytokine release, cellular cytotoxicity, and antigen presentation are impaired. FcγRI−/− mice showed impaired hypersensitivity responses, strongly reduced cartilage destruction in an arthritis model, and impaired protection from a bacterial infection. We conclude that FcγRI co...
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