Therapeutic regulation of the complement system in acute injury states.
The study of the intrinsic regulation of complement has uncovered a broad array of proteins with differing specificities and physicochemical properties. This will allow application of these proteins, native or modified, to the problem of controlling inflammation. The availability of sCR1, as the first such agent, has permitted further definition of those adverse clinical situations which are complement-dependent. The use of sCR1 as a drug might be anticipated in situations of thermal injury, ARDS, septic shock, and ischemia/reperfusion injury, such as myocardial infarction after thrombolytic therapy. sCR1 may also serve as the tool with which to unravel and possibly treat xenograft rejection. It can be anticipated that other such specific inhibitors will become available.
Moore
F D
FD
Department of Surgery, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115.
D000818:Animals; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D003167:Complement Activation / Q000276:immunology*; D003169:Complement Inactivator Proteins / Q000276:immunology*; D003165:Complement System Proteins / Q000172:deficiency; D006084:Graft Rejection / Q000276:immunology; D006801:Humans; D007962:Leukocytes / Q000276:immunology; D006435:Renal Dialysis / Q000009:adverse effects; D015427:Reperfusion Injury / Q000276:immunology; D012128:Respiratory Distress Syndrome / Q000276:immunology; D012772:Shock, Septic / Q000276:immunology; D014947:Wounds and Injuries / Q000276:immunology*
D003169:Complement Inactivator Proteins; D003165:Complement System Proteins