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CUTTING EDGE |
The Austin Research Institute, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia
Mouse IgG3 appears early in immune responses independently of T
cell help and, as such, is an early effector molecule of the immune
system. Yet, a specific IgG3 cellular receptor remains undefined. In
transfection experiments, mouse Fc
RI was clearly able to bind immune
complexes of IgG3, whereas mouse FcRII could not. Furthermore,
macrophages from mice expressing FcRII and FcRIII but lacking
FcRI were unable to phagocytose IgG3 immune complexes, thus
identifying mouse FcRI as the sole receptor for IgG3 immune
complexes. Competition studies demonstrated that monomeric mouse IgG3
could inhibit IgG2a binding to mouse FcRI with an
ID50 
10-7 M (fivefold lower than
IgG2a). The identification of mouse FcRI as the IgG3 receptor
establishes FcRI as a participant in events at the interface between
innate and adaptive immunity, implying a greater role for this receptor
in the development of normal and pathologic immune responses than
previously recognized.
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