The improved longer-term outcomes in CR2-fH-treated mice compared to CR2-Crry-treated and C3-deficient mice, and the inhibition of neurogenesis in CR2-Crry-treated and C3-deficient mice, indicate that CR2-fH provides targeted and self-limiting complement inhibition that dissects the dual role of complement in injury and recovery after stroke. Here, C3 is linked to Stroke.