Local and systemic inflammatory responses have been shown to play an
important role in post-stroke damage. Recent studies suggest that the innate immune
cells contribute to stroke-induced brain injury by activating an inflammatory response
that further increases local ischemic damage. Innate immune signaling, via Toll-like
receptors (TLRs), has been shown to be involved in several neuropathological
processes. This chapter summarizes the current knowledge concerning the involvement
of TLRs in acute ischemic brain injury. In particular, the therapeutic role of TLR2 and
TLR4 antagonists will be discussed. Moreover, since TLR3 stimulation could play a
beneficial role through the production of anti-inflammatory molecules, including I type
interferons (IFNs), the potential benefits of TLR3 agonist administration to counteract
stroke-related inflammation will be also focused.
Keywords: DAMPs, IFNα/β, Immunomodulators TLR-targeting, Inflammatory
Responses, Innate Immunity, Ischemia/Reperfusion, Pro-inflammatory Cytokines,
Stroke, TLR Agonists/Antagonists, TLRs.
