These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [The complement system].
    Author: Lambert PH.
    Journal: Schweiz Med Wochenschr; 1975 Sep 13; 105(37):1180-4. PubMed ID: 1215899.
    Abstract:
    The complement system may be activated by at least two different pathways: the clinical pathway involving C1, C4 and C2 and the alternative pathway involving properdin, C3, factor B and factor D. The classical pathway can be activated by antigen antibody complexes, while the alternative pathway can be activated by other substances such as natural polysaccharides. Both pathways lead to an activation of C3 and of the last complement components (C5 to C9). Congenital defects of the complement system have been described for several components. Some of these defects are relatively well tolerated, but others, such as C3 deficiency, lead to increased susceptibility to bacterial infections. Acquired complement defects are frequently observed in association with several diseases. Usually they are characterized by an increased level of complement components involved in the classical pathway and therefore reflect activation by antigen antibody complexes. Such changes may be systematic, as in lupus erythematodes, or localized to some biological fluids such as synovial fluid in rheumatoid arthritis. In some renal diseases the complement profile suggests activation of the complement system by the alternative pathway, and this may reflect a different pathogenesis.
    [Abstract] [Full Text] [Related] [New Search]