Table 2.
Studies of coagulation system factors: effects on neuroinflammatory processes using transgenic mice or pharmacological substances.
| Mouse line (genetic background) | Model (peptide) | Genetic background or species | Neuroinflammatory effect | Reference |
|---|---|---|---|---|
| γ377–395 | Active RR-EAE (PLP) | SJL | Reduced clinical symptoms, decreased inflammation, reduced microglial activation | (58) |
| Ancrod | Active RR-EAE (PLP) | SJL | Reduced clinical symptoms, decreased microglial activation and demyelination, no impact on immune cell proliferation | (58) |
| TNF-transgenic model (no peptide, spontaneous) | Tg6072 TNF transgenic mice | Reduced demyelination, downregulation of MHC-I | (60) | |
| Active EAE | Rat | Reduced clinical symptoms, decreased inflammation and fibrin deposition | (62) | |
| Batroxobin | Active EAE (MOG) | C57BL/6 | Reduced clinical symptoms, decreased inflammation, demyelination, no effect on axonal damage | (63) |
| AT-EAE (GP-MBP) | Rat | Attenuated disease course, reduced fibrin depositions, no effect on inflammation and immune cell proliferation | (64) | |
| ε-Aminocaproic acid | Active EAE | Rat | Attenuated disease course | (65) |
| Fibγ390–396A | Active EAE (MOG) | C57BL/6 | Reduced clinical symptoms, decreased inflammation, demyelination, reduced microglial activation | (58) |
| Hirudin | Active EAE (PLP) | SJL/J | Improvement of clinical deficits, reduced inflammation, decreased immune cell proliferation and cytokine production | (13) |
| PAI-1−/− | Active CREAE (spinal cord homogenate) | ABH | Reduced incidence, moderately delayed onset, reduced inflammation, no effect on demyelination and axonal damage | (39) |
| PAI-1-dp (uPA activator) | Active EAE (MOG) | C57BL/6 | Attenuated disease course, reduced Tcell proliferation and cytokine production | (38) |
| TgK21fib−/− | TNF-transgenic model (no peptide, spontaneous) | Increased lifespan, delayed onset of clinical symptoms, reduced inflammation and demyelination | (60) | |
| tPA−/− | Active EAE (MOG) | C57BL/6 | Aggravated disease course, enhanced demyelination, axonal damage, fibrin deposition | (39) |
| Delayed disease onset, aggravated disease course, delayed, but prolonged demyelination and axonal damage, reduced microglial activation | (66) | |||
| uPA−/− | Active EAE (MOG) | C57BL/6 | Aggravated disease course, enhanced inflammation and microglial activation | (38) |
AT, adoptive transfer; CREAE, chronic relapsing experimental allergic encephalomyelitis; EAE, experimental autoimmune encephalomyelitis; MHC-I, major histocompatibility complex class I; MOG, myelin oligodendrocyte glycoprotein; PAI-I, plasminogen activator inhibitor I; PAI-I-dp, plasminogen activator inhibitor I-deprived; PLP, proteolipid protein; TNF, tumor necrosis factor; tPA, tissue plasminogen activator; uPA, urokinase plasminogen activator; RR, relapsing–remitting.