| 摘要 |
If pathogen factors such as meningococcal NMB 1870 or flaviviral NS1 are able to sequester factor H in the blood then its inhibitory effect on complement may be disturbed, thereby permitting C3 to initiate a dramatic attack on host endothelial tissue. In combination with a strong inflammatory response, this attack can result in sever damage to the endothelium, with resulting hemorrhagic syndrome. Blocking the interaction between pathogen factors and factor H may thus be used to treat and/or prevent these pathogen-induced hemorrhagic syndromes. The interaction may, for instance, be blocked by antibodies, either delivered endogenously (passive immunisation) or produced by a patient's immune system (active immunisation).
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