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The Journal of Immunology, 2002, 168: 2011-2019.
Copyright © 2002 by The American Association of Immunologists

G-CSF Therapy of Ongoing Experimental Allergic Encephalomyelitis Via Chemokine- and Cytokine-Based Immune Deviation

Flora Zavala1,*, Sébastien Abad*, Sophie Ezine{dagger}, Véronique Taupin{ddagger}, Annie Masson* and Jean-François Bach*

Institut National de la Santé et de la Recherche Médical, * Unité 25 and {dagger} Unité 345, Necker Hospital, Paris, France; and {ddagger} Sanofi-Synthelabo, Bagneux, France

Converging evidence that G-CSF, the hemopoietic growth factor of the myeloid lineage, also exerts anti-inflammatory and pro-Th2 effects, prompted us to evaluate its direct therapeutic potential in autoimmune diseases. Here we report a novel activity of G-CSF in experimental allergic encephalomyelitis, a murine model for multiple sclerosis, driven by Th1-oriented autoaggressive cells. A short 7-day treatment with G-CSF, initiated at the onset of clinical signs, provided durable protection from experimental autoimmune encephalomyelitis. G-CSF-treated mice displayed limited demyelination, reduced recruitment of T cells to the CNS, and very discrete autoimmune inflammation, as well as barely detectable CNS mRNA levels of cytokines and chemokines. In the periphery, G-CSF treatment triggered an imbalance in the production by macrophages as well as autoreactive splenocytes of macrophage inflammatory protein-1{alpha} and monocyte chemoattractant protein-1, the prototypical pro-Th1 and pro-Th2 CC chemokines, respectively. This chemokine imbalance was associated with an immune deviation of the autoreactive response, with reduced IFN-{gamma} and increased IL-4 and TGF-{beta}1 levels. Moreover, G-CSF limited the production of TNF-{alpha}, a cytokine also associated with early CNS infiltration and neurological deficit. These findings support the potential application of G-CSF in the treatment of human autoimmune diseases such as multiple sclerosis, taking advantage of the wide clinical favorable experience with this molecule.




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