Systemic lupus erythematosus and complement.
SLE is characterized by a host of immune abnormalities. It is not clear to date which of these are primary and which are secondary. The observation of a number of genetic defects suggests that they are primary. Multiple genetic defects may then lead to abnormal immune responses to common pathogens, antigens, or even autoantigens. As a result of this abnormal immune response, immune complexes form with resultant complement fixation and activation. These immune complexes interacting with cells and complement initiate an inflammatory response. One can also speculate that this inflammatory response represents a normal response to an abnormal event, or is also abnormal in the SLE patient. The ultimate result is tissue inflammation and often damage. While at present our therapy is aimed at controlling these secondary inflammatory phenomena mediated by immune complexes and complement, ultimately therapy may be more successful after the primary defects are corrected.
D003167:Complement Activation; D003165:Complement System Proteins / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D005122:Exudates and Transudates / Q000276:immunology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D010490:Pericardial Effusion / Q000276:immunology; D010996:Pleural Effusion / Q000276:immunology; D013582:Synovial Fluid / Q000276:immunology
D003165:Complement System Proteins