Stroke kills 15 million people a year and causes disabilities in many more millions who survive. Most strokes are caused by a blood clot, yet only seven percent of patients qualify for early pharmacological clot removal. Damage is frequently exacerbated even as blood reperfuses an ischaemic brain region, through a concomitant inflammatory response to the damaged tissue. Following the continual failure in clinical trials of drugs intended to tackle both initial excitotoxic cell death and pro-­‐inflammatory mechanisms during ischaemia/reperfusion (I/R), this thesis is premised on enhancing 'pro-­‐resolving' anti-­‐inflammatory pathways. Formyl Peptide Receptor 2/the lipoxin receptor (FPR2/ALX; mouse orthologue Fpr2/3) and two of its ligands, Lipoxin A4 (LXA4) and Annexin A1 (AnxA1), are part of an endogenous anti-­‐ inflammatory system. They actively resolve inflammation through a reduction in characteristic leukocyte-­‐endothelial (L-­‐E) interactions, while promoting the production of anti-­‐inflammatory cytokines and non-­‐phlogistic phagocytosis of leukocytes already within tissue. Chapters 3-­‐5 of this thesis describe the development of mouse model of global cerebral I/R (5 min ischaemia/40 min or 2 h reperfusion) through which L-­‐E interactions are assessed using intravital microscopy. Substantial reductions in L-­‐E interactions following treatment with FPR2/ALX ligands (AnxA1 N-­‐ terminal peptide AnxA1Ac2-­‐26 and LXA4 analogue 15-­‐epi-­‐LXA4) are demonstrated along with variations in cytokine levels (MCP-­‐1, IL-­‐6 and IL-­‐10) after 2 h of reperfusion. The reductions are shown to be variable with respect to the duration of reperfusion, concentration of 15-­‐epi-­‐LXA4 and the time of treatment administration. In addition, the effects are abrogated by co-­‐treatment with FPR antagonists, which independently cause a highly pronounced acute inflammatory response in the model. Chapters 6 and 7 provide further investigation into the role of FPRs in stroke and inflammation, through chemotaxis studies on human monocytes (from stroke patients and healthy controls) and through use of an FPR1-­‐target MRI contrast agent in mice following lipopolysaccaride-­‐induced inflammation. Overall, the data provide evidence that Fpr2/3 ligands are able to reduce inflammation following cerebral I/R, that an FPR2/ALX-­‐targeted drug may therefore be effective in human stroke, and that its optimal use is likely to be administration time, dose and FPR2/ALX ligand-­‐dependent.