CVDs | ||||
---|---|---|---|---|
TLRs | AIS | ICH | SAH | CVST |
TLR2 | Moderator for leukocytes and microglial infiltration and neuronal death [78, 79] | – | Activated in antiphospholipid syndrome [80] | |
TLR3 |
Neuroprotective and anti-inflammatory effects on SD-induced neuroinflammation [63] Ischemic tolerance induction by TLR3 ligand poly I:C preconditioning through type I IFN signaling [81] | Neuroprotective and anti-inflammatory effects on SD-induced neuroinflammation [21, 82] | ||
TLR4 |
Neuroprotective effect by preconditioning through suppression of cytotoxic TNFα, increasing IRFs and production of type I interferons [78, 79] Induction and evolution of atherosclerosis through NF-κB pathway that produce inflammation [78, 79] | Increasing levels of inflammatory factors, DNA damage, and neuronal degeneration in perihematomal region [82] | Activation by Heme product through the MyD88 and TRIF pathways [83] | Activated in antiphospholipid syndrome [80] |
TLR7 | Neuroprotective effect by preconditioning with TLR7 ligand, gardiquimod, reduction in infarct size, and a better functional outcome independent of TNFα and dependent on interferon [84] | – | ||
TLR8 | Activation causes worsening of ischemic brain injury [85] | – | – | |
TLR9 | Neuroprotective effect by preconditioning through suppression of cytotoxic TNFα, increasing IRFs, and production of type I interferons [20] | – | Deletion is associated with larger venous thrombosis and increased leukocyte infiltration [80] |