Furthermore, as these experiments were primarily designed to elucidate the mechanisms C3a/C3aR-mediated injury, we did not perform post-ischemic dosing regimens, which are ultimately critical for translation of anti-complement strategies. Additionally, as neurofunctional recovery and neurogenesis continue into the chronic phase of stroke, further work is necessary to definitively establish the role for C3a/C3aR in neurorecovery at later post-ischemic time-points. In conclusion, despite reports of a positive regulatory role for complement in neurogenesis, targeted complement inhibition through low-dose antagonism of the C3a receptor actually promotes the proliferation of migrating neuroblasts in the SVZ following reperfused stroke. Furthermore, C3aR is expressed by infiltrating T-lymphocytes in the ischemic region at 7 days postischemia, and C3aRA administration attenuates the infiltration of these cells. Additionally, the functional and histologic neuroprotection associated with C3aRA administration is sustained when evaluated at an extended time-point. Although further work is necessary to characterize the mechanisms of complement-mediated inflammatory signaling and its effect on post-ischemic neurogenesis, as well as the relationship between neurogenesis and functional outcome, targeted pharmacologic inhibition of complement may ultimately represent an effective strategy for the treatment of stroke. Chronic hepatic inflammation from diverse causes including alcohol, steatohepatitis, autoimmune disease and viral infection leads to a wound healing, pro-fibrogenic response. In some patients with ongoing liver injury, this response can progress to cirrhosis, portal hypertension and liver failure. These outcomes are associated with a significant mortality rate for which liver transplantation is the only curative therapy. However, low donor numbers, high procedural costs and the requirement for life-long immunosuppression limit the number of patients who undergo transplantation and consequently alternative therapies have been sought. Among these, the transplantation of Vismodegib hematopoietic and mesenchymal stem cells derived from adult bone marrow and placenta have shown beneficial effects in animal models of hepatic fibrosis leading to early phase clinical trials using autologous bone marrow derived cells. Most of the clinical trials have been small, often with less than ten patients, and uncontrolled but have shown short-term clinical benefits. Recently, we have shown that transplantation of placenta derived human amniotic epithelial cells into immunocompetent mice with carbon tetrachloride induced liver fibrosis can constrain hepatic fibrogenesis. This outcome may be related to several factors linked to hAEC transplantation including reduction in the expression of pro-inflammatory and pro-fibrogenic cytokines coupled with the induction of matrix metalloproteinases to promote a collagen-degrading environment. During pregnancy, hAEC form a monolayer lining the inner of two membranes retaining the amniotic fluid surrounding the fetus.