Immunoglobulin Fcγ receptors (FcγR) are comprised of a ligand-binding α-chain that sometimes associates with a cell signaling common γ-chain. These receptors comprise an important family of effector molecules that link humoral and cell-mediated adaptive immunity and regulate innate immunity. Recent animal studies suggest that FcγR in general, and FcR α-chains in particular, are required for full development of experimental autoimmune encephalomyelitis (EAE). We show here that deletion of the γ-chain renders mice resistant to EAE, whereas deletion of the α-chains of FcγRI, FcγRIIB and FcγRIII has no protective effect. Susceptibility to EAE is fully restored in common γ-chain-/- mice into which wild-type splenocytes are adoptively transferred, but EAE is not restored in common γ-chain-/- mice given wild-type splenocytes depleted of γδ T cells. These data indicate that although the common γ-chain is required for full development of EAE in mice, this requirement is likely FcγR α-chain-independent. Expression of the common γ-chain by γδ T cells, probably in conjunction with the T cell receptor/CD3 complex, is likely the key requirement for full development of EAE. © 2005 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
