Serum levels of C3-activator (antifactor B) in leprosy.
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Complement Activating Enzymes↗
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Conversion of the C3 component of complement in mice infected with Trypanosoma cruzi.
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Animals↗
Lymphocyte traffic through antigen-stimulated lymph nodes. I. Complement activation within lymph nodes initiates cell shutdown.
Complement activation within lymph nodes has been shown to alter lymphocyte traffic through the node. Challenge of cannulated sheep lymph nodes with either immune complexes or complement activators was found to initiate the phenomenon of cell shutdown associated with antigenic challenge of lymph nodes in primed animals.
Animals↗
[Does temperature in extracorporeal circulation affect neutrophil-endothelium interactions?].
The increasing interest in "warm" aerobic cardioplegia requires a critical reevaluation of the systemic effects of the associated normothermic cardiopulmonary bypass (CPB). As activated neutrophils seem to be essential mediators of the inflammatory response to CPB via the cytotoxicity of the products that are released during their adhesion to endothelial cells, the authors undertook a study of the influence of temperature on the interaction between the neutrophils and the endothelium in 95 patients undergoing warm (31-33.5 degrees C, n = 49) and cold (26-27 degrees C, n = 46) CPB surgery. Blood sampling was performed before, during and after CPB. The following markers of neutrophil-endocardium interaction were analysed: complement activation (C3a), cytokine production (tumor necrosis factor alpha, interleukines 1, 6 and 8, and interleukin-1 receptor antagonist); endothelial expression of cytokine-dependent [intercellular adhesion molecule (ICAM)] and cytokine-independent (P-selectin) adhesion molecules (P-selectin); expression of cytokine molecules on the surface of polynuclear neutrophils (CD11a, CD11b, CD11c); and finally, endothelial adhesion and transendothelial migration of neutrophils (interleukin 8 and elastase). The results showed that, irrespective of temperature, CPB was associated with changes strongly suggestive of phenomena of transendothelial adhesion and migration. Moreover, normothermia increased the intensity of the inflammatory response as shown by increased cytokine production, earlier expression of neutrophil adhesion molecules and increased elastase production.
Aged↗
Active sites in complement component C3 mapped by mutations at indels.
Engineered mutants of human complement component C3 were used to test the idea that sites of length polymorphisms in protein families (indels) can guide a search for protein:protein interaction sites. Sequence changes were introduced at each of the 27 indels in the C3/4/5 protein family, and mutants at 26 indels were expressed by transiently transfected COS cells. Expressed proteins were assayed 1) for concentration, by ELISA and by autoradiography of radiolabeled protein; 2) for classical pathway hemolytic activity; 3) for susceptibility to proteolytic activation by the alternative pathway and cobra venom factor C3 convertases; and 4) for susceptibility to complement factor I in the presence of factor H. Most of the mutations did not appreciably alter expression or activity relative to wild-type C3, consistent with the idea that most indels occur at the protein surface. Mutations at four indels severely damaged C3 functional activity, but did not affect the stability or structure of the protein, as assessed by their effects on expression by COS cells and on susceptibility to cleavage by C3 convertases and factor I. These indels are therefore near functionally important amino acid residues; they represent good candidates for sites of protein:protein interactions. Mutation of the sequence at a fifth indel altered the equilibrium between the latent and reacted C3 conformations, and mutations at 4 other indels substantially decreased both protein activity and expression. The mutants provided an overview of the structural and functional roles played by different parts of C3.
Amino Acid Sequence↗
Complement activation in renal disease.
Perturbation of the serum complement system in glomerulonephritis can be the result of classical pathway activation by immune complexes or of C3 activation by the C3-C5 convertase stabilized by the C3 nephritic factor. Low C3 levels can also be the result of diminished C3 synthesis and possibly, in certain circumstances, of C3 convertases deposited on capillary walls. In glomerulonephritis the complement profile is helpful in diagnosis, in following the course of therapy and in providing insights into pathogenesis. Complement profiles must be interpreted recognizing that a pattern resembling classical pathway activation can be produced by idiopathic nephrotic syndrome, that hypogammaglobulinemia can reduce Clq levels, and that a primary deficiency of factor H or I or both, will secondarily produce subnormal levels of C3 and factor B. With these caveats, the complement profiles typical of systemic lupus erythematosus, membranoproliferative glomerulonephritis, acute glomerulonephritis, acquired Cl inhibitor deficiency, and hypocomplementemic vasculitis syndrome are described.
Antigen-Antibody Complex↗