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Vascular response is central to many forms of repair-associated research

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EAE studies using neutralizing antibodies against CCL2 and CCL3 suggested that CCL3 controls accumulation of mononuclear cell during acute EAE, correlating with increasing acute disease severity, while CCL2 was responsible for a mononuclear cell infiltration during relapsing EAE (Karpus et al., 1995