Inflammation is a key process linked to stroke both in terms of atherosclerosis, and in terms of cerebral ischaemia. Secondary to endothelial injury, innate and acquired immune mechanisms maintain a chronic low-grade inflammatory state, which initially contributes to formation of atherosclerotic plaques, and ultimately leads to detrimental complications, such as rupture and thrombosis. Experimental models of cerebral ischaemia have shown that inflammatory immune cascades mediate ischaemia/reperfusion injury, and therefore, could be strongly related to stroke outcome. In the case of atherosclerosis and ischaemic stroke, the pro-inflammatory (Type-1) cytokines predominate over their counterparts, the anti-inflammatory (Type-2) cytokines. Elevated plasma levels of Type-1 cytokines have been associated with unstable atherosclerotic plaques and risk of stroke, while Type-2 cytokines seem to relate with better functional outcome after stroke. Multiple genetic variations (e.g. single nucleotide polymorphisms) have been identified in the genes of these molecules, some of which seem to regulate their transcription rate, or their functionality. The association of these genetic variants with risk of stroke and post-stroke functional outcome has been extensively investigated. We systematically review polymorphisms of inflammatory cytokines associated with ischaemic stroke, in respect to their immune type (Type-1 or 2), and provide possible implications for stroke prevention, therapy and future research.