Stroke is the leading cause of death and the main cause of disability in surviving patients. The detrimental interaction between immune cells, glial cells, and matrix components in stroke pathology results in persistent inflammation that progresses to fibrosis. A substantial effort is being directed toward understanding the exact neuroinflammatory events that take place as a result of stroke. The initiation of a potent cytokine response, along with immune cell activation and infiltration in the ischemic core, has massive acute deleterious effects, generally exacerbated by comorbid inflammatory conditions. There is secondary neuroinflammation that promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. This highlights the need for a better understanding of the neuroinflammatory and fibrotic processes, as well as the need to identify new mechanisms and potential modulators. In this review, we summarize several aspects of stroke-induced inflammation, fibrosis, and include a discussion of cytokine inhibitors/inducers, immune cells, and fibro-inflammation signaling inhibitors in order to identify new pharmacological means of intervention.