We constructed an immunotoxin, composed of an antibody directed against the
high-affinity IgG receptor CD64 and Ricin-A, with the aim of resolving chr
onic inflammation through elimination of activated macrophages, In vitro, t
his immunotoxin proved very efficient in inducing apoptosis in activated ma
crophages, leaving resting and low CD64-expressing macrophages unaffected.
We examined the activity of our immunotoxin in a sodium lauryl sulfate (SLS
)-induced cutaneous inflammation model, using transgenic mice expressing hu
man CD64. Upon intradermal injection of the immunotoxin (IT), cutaneous inf
lammation resolved in 24 h. This was demonstrated histologically by clearan
ce of all CD64-expressing macrophages, followed by clearance of other infla
mmatory cells. Clinical parameters associated with inflammation, such as lo
cal skin temperature and vasodilation, also decreased.