The inflammatory response, by disrupting immunohomeostasis and aggravating brain damage, constitutes a major contributory factor to the pathobiology of stroke. Because the immune system is involved in all stages of stroke, immunosuppressive mechanisms may provide neuroprotection in this setting. The TAM/Gas6 pathway, for instance, has been shown to be involved in modulating post-stroke inflammation, and in the reduction of post-stroke brain injury. In addition to this pathway, those mediated by established immunosuppressive molecules (such as IL-10 and TGF-β), by CD25⁺CD4⁺ FoxP3⁺Tregs, and by the cholinergic anti-inflammatory pathway, also appear to play protective roles in the context of stroke. Taken together, evidence accumulated regarding the function of these mechanisms suggest than an immunoregulatory strategy may prove promising, both as an approach to the study of stroke pathophysiology, and to the discovery of treatments that limit the destructive effects of cerebrovascular disease.