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*
Institut National de la Santé et de la Recherche Médicale Unité 25,
Unité 345, and
Centre National de la Recherche Scientifique Unité Mixte de Recherche 8603, Hôpital Necker, Paris, France
G-CSF not only functions as an endogenous hemopoietic growth factor
for neutrophils, but also displays pro-Th2 and antiinflammatory
properties that could be of therapeutic benefit in autoimmune settings.
We evaluated the effect of treatment with G-CSF in a murine model of
spontaneous systemic lupus erythematosus, a disease in which G-CSF is
already administered to patients to alleviate neutropenia, a common
complication. Chronic treatment of lupus-prone
MRL-lpr/lpr mice with low doses (10 µg/kg) of
recombinant human G-CSF, despite the induction of a shift toward the
Th2 phenotype of the autoimmune response, increased glomerular
deposition of Igs and accelerated lupus disease. Conversely, high-dose
(200 µg/kg) treatment with G-CSF induced substantial protection,
prolonging survival by >2 mo. In the animals treated with these high
doses of G-CSF, neither the Th1/Th2 profile nor the serum levels of
TNF-
and IL-10 were modified. Despite the presence of immune
complexes in their kidney glomeruli, no inflammation ensued, and serum
IL-12 and soluble TNF receptors remained at pre-disease levels. This
uncoupling of immune complex deposition and kidney damage resulted from
a local down-modulation of Fc
RIII (CD16) expression within the
glomeruli by G-CSF. Our results demonstrate a beneficial effect of high
doses of G-CSF in the prevention of lupus nephritis that may hold
promise for future clinical applications, provided caution is taken in
dose adjustment.
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