Requirement of the Fc receptor common γ-chain forγδ T cell-mediated promotion of murine experimental autoimmune encephalomyelitis

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Abstract
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.