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PubMed2004

Beyond C4d: other complement-related diagnostic approaches to antibody-mediated rejection.

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.

Animals↗
PubMed1977

C1 subcomponents in acute pneumococcal otitis media in children.

Twenty children with acute pneumococcal otitis media were studied. In 6 children the infection ran a normal course and healed after the first episode and in 14 it relapsed. The serum levels of the immunoglobulins IgG, IgA and IgM were normal in all 20 children. Specific antibodies to pneumococcal polysaccharide were found in all cases, with no differences in the titers between the relapsed cases and those that healed. The complement components were quantitated with electroimmuno assay. G1q proved depressed in 60 per cent of the relapsed cases and in 16 per cent of the healed cases. C1r and C1s were disproportionally high compared with the C1q levels. Furthermore, crossed immunoelectrophoresis revealed abnormal complexes composed of C1r and C1s, and complexes composed of C1r, C1s and C1 IA. These complexes were more pronounced in sera from the children with relapsing otitis media.

Acute Disease↗
PubMed1987

Heterogeneity of C4d and C3d and their complex formation with serum albumin.

High molecular weight (Mr around 175 KD) forms of C4d and C3d as well as free C4d and C3d (Mr about 40 KD) were demonstrable in normal human serum (NHS). Following in vitro C activation in NHS by delta IgG, the 40 KD C4d component increased markedly. By immunofixation it was shown that the high molecular forms of C4d and C3d reacted with biotinylated anti-human albumin IgG, whereas the 40 KD-free C4d and C3d fragments did not. Furthermore, the incorporation of anti-albumin IgG in the first dimensional gel in crossed immunoelectrophoresis caused retention of the 175 KD C4d component but not of free C4d. The 175 KD C4d had a distinctly higher electrophoretic migration velocity (post-albumin region) than the 40 KD C4d fragment. The C3d-, C4d-serum albumin complexes could not be dissociated by reducing agents (DTT, mercaptoethanol), a non-ionic detergent, or exposure to high and low ionic strength.

Complement Activation↗
PubMedDate not supplied

Report of studies on monoclonal antibodies (MABS) to complement components.

Twenty-five monoclonal antibodies (MABS) to complement components were evaluated according to the ISBT/ICSH protocol by twelve laboratories. Seven detected some form of C3c, but one of them, 174, did not react with EiC3b, although it was positive with 'EC3b' (Fruitstone). 174 may detect some form of enzyme sensitive C3b antigen, but C3a was not evaluated (present on 'EC3b' Fruitstone). Twelve of the antibodies were anti-C3d, one was an anti-C3g and five were anti-C4c.

Antibodies, Monoclonal↗
PubMed1976

Modulation of C3b hemolytic activity by a plasma protein distinct from C3b inactivator.

A human plasma protein binds to cell-bound C3b, the major cleavage product of the third component of complement. Consequent upon this binding, C3b no longer functions in either the classical or alternative pathways. This C3b inhibitory activity is a property of a protein previously designated beta 1H on the basis of its electrophoretic mobility.

Blood Proteins↗
PubMed1977

Interactions of radio-detoxified Escherichia coli endotoxin preparations with the complement system.

Escherichia coli O89 lipopolysaccharide (LPS) was treated with different doses of gamma irradiation (5, 10, 15, and 20 Mrad). Various biological activities such as lethal effect, decrease in arterial blood pressure in dogs, and interaction with the complement system were determined for the parent and irradiated preparations. Irradiation of LPS significantly and in a dose-dependent manner decreased its lethal and blood pressure-depressing effects along with its ability to activate the complement system. In contrast, radio-detoxified LPS fixed more strongly the isolated human C1 than did the parent LPS. The possible connection between the toxicity of endotoxin and endotoxin-induced complement activation is discussed.

Animals↗
PubMed1979

In vitro synthesis of humoral factors (immunoglobulins and complement) in lesional skin of leprosy patients.

An in vitro culture technique was used to demonstrate the synthesis of immunoglobulins and complement in lesional skin of patients representing the entire clinico-histopathological spectrum of leprosy. The results indicate that immunoglobulin G is produced in different amounts in the various forms of leprosy. Classification of the patients according to the three main groups shows that a small amount of immunoglobulin G synthesis occurred in tuberculoid leprosy, a distinct amount occurred in borderline leprosy, and large amount occurred in lepromatous leprosy. Contrary to expectation, synthesis of C3 was found only in some of the cultures of these three forms of leprosy. The function of the locally synthesized immunoglobulin G and the findings concerning C3 synthesis are discussed.

Adolescent↗
PubMed1980

Experimental Chagas' disease in complement-deficient mice and guinea pigs.

The course of infection with trypomastigotes of Trypanosoma cruzi (House 510 strain) in mice and guinea pigs with genetic complement deficiencies was compared with that in normocomplementemic animals. Parasitemias in a mouse strain (B10.D2/old) genetically deficient in C5 and therefore unable to sustain lysis were similar to or lower than in a congenic normocomplementemic strain (B10.D2/new). The levels of C3 measured immunochemically were generally unaffected. There were no significant differences in mortality rates. These results indicate that, in mice, complement-mediated lysis does not play a significant role in the control of T. cruzi (House 510) infections. Studies were also performed in normocomplementemic guinea pigs and in guinea pigs genetically deficient in the fourth component of complement and thus unable to support functions mediated by the classical pathway of complement activation. No significant differences were noted between the two strains in the course of infection, persistence of subpatent infection, or rate of mortality, indicating that if the classical complement pathway plays a role in resistance to T. cruzi (House 510) in guinea pigs, this role must be a small one.

Animals↗
PubMed1992

Legionella pneumophila lipopolysaccharide activates the classical complement pathway.

Legionella pneumophila is a gram-negative bacterium capable of entering and growing in alveolar macrophages and monocytes. Complement and complement receptors are important in the uptake of L. pneumophila by human mononuclear phagocytes. The surface molecules of L. pneumophila that activate the complement system are unknown. To identify these factors, we investigated the effects of L. pneumophila lipopolysaccharide (LPS) on the classical and alternative complement pathways of normal human serum by functional hemolytic assays. Although incubation of LPS in normal human serum at 37 degrees C resulted in the activation of both pathways, complement activation proceeded primarily through the classical pathway. Activation of the classical pathway by LPS was dependent on natural antibodies of the immunoglobulin M class that were present in various quantities in sera from different normal individuals but were absent in an immunoglobulin-deficient serum obtained from an agammaglobulinemic patient. Additional studies using sheep erythrocytes coated with LPS suggested that the antibodies recognized antigenic sites in the carbohydrate portion of LPS. The ability of LPS to interact with the complement system suggests a role for LPS in the uptake of L. pneumophila by mononuclear phagocytes.

Complement C1↗
PubMed2000

Treponema pallidum subsp. pertenue displays pathogenic properties different from those of T. pallidum subsp. pallidum.

The present study described the susceptibility of C4D guinea pigs to cutaneous infection with Treponema pallidum subsp. pertenue Haiti B strain. The general manifestations of the disease in adults and neonates differ, to a certain degree, from those induced by T. pallidum subsp. pallidum Nichols strain. Noticeable differences between the infections were reflected in the character of the skin lesions, their onset and persistence, and the kinetics of the humoral response. The incidence and dissemination of cutaneous yaws lesions in very young guinea pigs were remarkably different from the low frequency observed in a similar age group of syphilis infection, 100 versus 17%, respectively. Moreover, as opposed to T. pallidum subsp. pallidum, T. pallidum subsp. pertenue does not cross the placenta. Offspring born to yaws-infected mothers did not produce immunoglobulin M antibodies and their organs, examined by PCR and rabbit infectivity test (RIT), were all negative. Examination of a large number of tissues and organs in adult, neonate, and maternal yaws by PCR and RIT clearly demonstrated that, unlike syphilis, there was a low incidence and short persistence of the yaws pathogen in internal organs. These findings stress the dermotropic rather than the organotropic character of yaws and provide further evidence of distinctive biological and pathological differences between yaws and venereal syphilis.

Age Factors↗