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PubMed1979

[Complement: function. Biological significance and clinical aspects (author's transl)].

The term complement comprises approximately twenty serum proteins. Activation of these components can be started by antigen-antibody complexes or even without the participation of antibodies. The activated complement proteins bring about a number of important biological actions. They produce vigorous local inflammatory reactions, exert phagocytosis--increase effects, destroy microbial and animal cells and affect the immune response to antigen stimulus. Congenital lack of individual complement components may considerably impair the antimicrobial defense or even be the cause of excessive inflammatory reactions. The activation of complement may also have harmful effects on the organism.

Angioedema↗
PubMed2003

[Investigation of the complement system in clinical practice].

The complement system plays an important role in defence of the host against infection and in the clearance of immune complexes. Defects in complement proteins are often associated with infections or auto/immune complex diseases. Investigation of complement is useful for diagnosis and following of auto-immune diseases. The aim of this Article is to provide an overview of important applications of complement in medicine, emphasizing the role of complement in pathogenesis and the usefulness of measurements of complement proteins in diagnosis and assessment of the evolution of disease states. Emphasis has been placed on practical applications and understanding basic mechanisms of disease. The best screen for complement deficiencies or significant activation is the CH50, which measures total classical pathway activity and the measurement of C3 and C4. The absence or decrease of multiple components is usually due to consumption of complement. Complete lack of CH50 associated with normal C3 antigen is a strong indication for complement deficiency and should be followed up with further tests to determine which component is missing.

Angioedema↗
PubMed1992

The role of the mucosal immune system in inflammatory bowel disease.

Continued delineation of the major factors that lead to intestinal inflammation will provide critical insights into many of the pathophysiologic events leading to tissue destruction in IBD. The exploration of exciting and important new areas, such as the role of adhesion molecules, proinflammatory cytokines, and the activation of lymphocytes and phagocytes, will contribute significantly to a better understanding of the mechanisms that sustain the intestinal inflammatory process. Determining the mechanisms of amplification and perpetuation of intestinal inflammation as well as learning more about the natural suppression of intestinal inflammation by the normal cellular and cytokine networks of the mucosal immune system will open exciting new therapeutic approaches. It is encouraging to see realistic and testable working models emerge from the combined efforts of many committed investigators who have been engaged in studying the role of the mucosal immune system in the pathophysiology of IBD. A great deal more remains to be learned in this rapidly advancing area, and we can look forward with confidence to continued advances in the study of IBD.

Antibody Formation↗
PubMed1991

A covalent dimer of complement C4b serves as a subunit of a novel C5 convertase that involves no C3 derivatives.

A C intermediate, LAC14, was prepared from TNP-aminocaproyl liposomes sensitized with anti-TNP antibody (Ab) and purified human C1 and C4. LAC14, containing radiolabeled C4, was analyzed by SDS-PAGE followed by autoradiography, and yielded a 210-kDa band and a predominant 400-kDa band. The 210-kDa band consisted of monomeric C4b bound to low molecular mass acceptors. The 400-kDa band was comprised of a 200-kDa moiety, as well as beta- and gamma-chains of C4. The 200-kDa moiety contained neither C1 nor sensitizing Ab, but it was largely decreased by treatment with NH2OH to the 90-kDa moiety with the mobility corresponding to the alpha'-chain of C4b. A covalent dimer of C4b, therefore, is the predominant form of C4b deposited on liposomes sensitized with antibody. The C4b-C4b dimer formed rapidly (within 5 min) followed by slow dissociation into monomers. The LAC14 bearing the C4b dimer but not the monomer was lysed, although with relatively low efficiency, by the addition of oxyC2 and EDTA-supplemented C3-deficient serum (C3DS), and, furthermore, LAC142 possessed the ability to convert C5 into C5a and C5b. Moreover, lysis was inhibited not by anti-C3 Ab but by anti-C4 Ab. In other experiments, the dimer served as an element of C3 convertase, as well. These findings imply that the C4b dimer, when complexed with C2, expresses C3/C5 convertase activity without participation of C3, and may provide a molecular mechanism whereby sera from patients with complete C3 deficiency retain the ability to induce C-mediated cytolysis.

Autoradiography↗
PubMed1990

Biological and immunological properties of Sugi basic protein-pullulan conjugate. II. Is the reduced ability to elicit the Arthus reaction based on the poor activation of complement by immune complex consisting of anti-Sugi basic protein and Sugi basic protein-pullulan?

Ability of Sugi basic protein (SBP)-pullulan conjugate to elicit the Arthus reaction was found to be markedly reduced, about 100 times lower than that of native SBP. To analyze this reduced ability, activation of complement by immune complex consisting of SBP-pullulan and anti-SBP antibodies was studied. Tests for complement consumption, C3 conversion and cleavage of factor B revealed that immune complex formed with SBP-pullulan is incapable of supporting efficient activation of the complement system. Previously, we have shown data suggesting that SBP-pullulan conjugate would be a good candidate for desensitization therapy against cedar pollinosis. The results presented in this paper provide additional support for the suggestion.

Allergens↗