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Beyond C4d: Other Complement‐Related Diagnostic Approaches to Antibody‐Mediated Rejection
Author(s) -
Baldwin William M.,
Kasper Edward K.,
Zachary Andrea A.,
Wasowska Barbara A.,
Rodriguez E. Rene
Publication year - 2004
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2004.00348.x
Subject(s) - complement receptor , complement system , immunology , receptor , pathogenesis , innate immune system , effector , acquired immune system , antibody , complement component 3 , complement (music) , inflammation , complement receptor 1 , medicine , immunity , immune system , biology , gene , genetics , phenotype , complementation
Complement is a multifunctional system of receptors and regulators as well as effector molecules. Both the pathogenic and diagnostic power of complement is based on the capacity of the complement system to amplify innate and adaptive immunity. This amplification is accomplished through two strategies: ( 1 ) enzymatic reactions in the complement cascade, and ( 2 ) stimulation of leukocytes, platelets and parenchymal cells through specific receptors or receptor‐independent pore formation. The mechanisms by which complement mediates and modifies nonspecific inflammation, antibody‐mediated injury and T‐cell responses are of particular significance to the pathogenesis of transplant rejection. Understanding the mechanisms by which complement integrates the interactions of leukocytes, platelets and parenchymal cells offers opportunities to further refine the diagnosis of rejection.