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PubMed1991

Elevated plasma levels of the immunosuppressive complement fragment Ba in renal failure.

The complement fragment Ba is a 33 kD activation product of factor B which suppresses human B-lymphocyte functions in vitro. We report that plasma levels of Ba are highly elevated in patients with chronic renal failure (4.84 +/- 3.58 micrograms/ml) and in patients with end-stage renal disease undergoing regular hemodialysis (16.1 +/- 6.1 micrograms/ml) as compared to normals (1.01 +/- 0.30 micrograms/ml). Ba levels were strictly correlated with the creatinine clearance. The urinary excretion of Ba was 165-fold higher in patients with tubular proteinuria than in normals. These results indicate that the kidney is the major catabolic site for Ba. In addition, direct evidence was obtained for an enhanced turnover of the alternative pathway of complement in renal failure that, although it appears to be less important than the renal retention of Ba, contributes to elevated Ba plasma levels in these patients. Ba concentrations in dialysis patients who responded to hepatitis B vaccination were significantly lower than in non-responders. Furthermore, the in vitro IgM synthesis by purified mononuclear cells was negatively correlated with Ba concentrations determined in the plasma of these patients. These results suggest that the accumulation of Ba contributes to the defective immune response in patients with renal failure.

Adult↗
PubMed1991

Complement-mediated inactivation of interferon-gamma in ELISA systems.

The recovery of a predetermined amount of interferon-gamma (IFN-gamma) added to normal serum was studied in two independent sandwich ELISA systems specific for rat and human IFN-gamma. In both assays the ELISA activity was rapidly lost in fresh but not in heat-inactivated (30', 56 degrees C) serum. Ninety percent of the initial activity had disappeared within 30 minutes upon incubation at 37 degrees C. Serum-mediated inhibition was not species-specific as the ELISA activity of rat IFN-gamma diminished equally well in rat and human sera. Inhibition was critically dependent on the isotype of the solid-phase monoclonal antibody (mAb) used in the ELISA systems. IgG1 and IgG2a mAbs efficiently inhibited the ELISA activity of IFN-gamma, whereas an IgA mAb was ineffective. The inhibition was not influenced by a wide variety of anti-proteolytic agents but was effectively blocked by anti-complementary substances or treatments directed to the first (C1) and third (C3) component of complement. Our results indicate that activation of the classical pathway of complement (CPC) and the concomitant covalent binding of C3 to the IFN-gamma molecule play a major role in the inhibitory process. It is concluded that reduction of the ELISA activity is attributable to diminished accessibility of the detector antibody for the IFN-gamma protein as a consequence of C3 binding.

Binding Sites↗
PubMed1991

The role of lipopolysaccharide in complement-killing of Aeromonas hydrophila strains of serotype O:34.

The role of lipopolysaccharide (LPS) in the susceptibility of Aeromonas hydrophila strains of serotype O:34 to non-immune human serum was investigated using isogenic mutants (serum-sensitive), previously obtained on the basis of phage resistance, and characterized for their surface components. The classical complement pathway was found to be principally involved in the serum-killing of these sensitive strains. LPS preparations from serum-resistant or serum-sensitive strains, or purified core oligosaccharides (low-molecular-mass LPS) inactivated both bactericidal and complement activity of whole serum, while the O-antigen molecules (high-molecular-mass LPS) did not. The results indicate that LPS core oligosaccharide composition contributes to complement resistance of A. hydrophila strains from serotype O:34 with moderate virulence.

Aeromonas hydrophila↗
PubMed1992

Significance of C3 nephritic factor (C3NeF) in non-hypocomplementaemic serum with membranoproliferative glomerulonephritis (MPGN).

C3NeF is an autoantibody of C3 convertase (C3bBb) and is often detected in the serum of hypocomplementaemic MPGN patients. Serum samples from 104 non-hypocomplementaemic MPGN patients (C3NeF) were studied. C3NeF, which cannot activate the alternative pathway, was found in the sera of 6 patients. We examined the C3NeF in purified IgG from five of the non-hypocomplementaemic serum samples (non-hypo C3NeF) and four hypocomplementaemic serum samples (hypocomplementaemic C3NeF) to determine why C3NeF does not induce C3 splitting and hypocomplementaemia. Purified IgG from non-hypo C3NeF stabilized EAC4b3bBb cells in a manner similar to IgG from hypocomplementaemic C3NeF in EDTA gelatin veronal buffer. However, the non-hypo C3NeF IgG did not stabilize C3 convertase (EAC4b3bBb cells) in the presence of control proteins (factors H and I), whereas the hypocomplementaemic C3NeF IgG did. The C3NeF in the hypocomplementaemic serum displayed two characteristics: (i) inhibition of intrinsic decay of Ce convertase (C3bBb); and (ii) inhibition of extrinsic decay by factors H and I. Although the C3NeF in the non-hypocomplementaemic sera did inhibit the intrinsic decay in a manner similar to the hypocomplementaemic C3NeF IgG, it did not inhibit the extrinsic decay. Due to the different characteristics of hypocomplementaemic C3NeF and non-hypo C3NeF in the serum samples, the non-hypo C3NeF did not activate C3. Therefore, we conclude that C3NeF exhibits a heterogeneity which is very important in relation to the pathogenesis of MPGN.

Complement C3 Nephritic Factor↗
PubMed1992

Autoimmune reactions in patients with M-component and peripheral neuropathy.

A study of 17 patients with autoimmune axonal or demyelinating peripheral neuropathy in combination with M-component is described. The M-component was associated with MGUS (monoclonal gammopathy of undetermined significance) in 12 patients, CLL in one patient, Waldenström's disease in one patient, and myeloma in three patients. Immunohistological examination with direct and indirect fluorescence showed binding of antibodies to nerve structures of the same class and light chain as seen in the M-component. In five cases of IgM M-component, the demyelinating neuropathy was caused by binding of the IgM M-protein and complement C3b to myelin-associated glycoproteins (MAG). In 12 cases with axonal neuropathy, binding of IgG to the connective tissue of the peri- and endoneurium was found in 50% of cases, IgM in five cases, and IgD in one case. None of the patients had central nervous system (CNS) symptoms. The clinical and therapeutic difficulties are discussed; only two patients with an acute course responded to immunosuppression. A marked co-expression of other autoimmune phenomena is interpreted in the light of cross-reactions between the autoantibody and similar tissue autoantigens.

Adult↗
PubMedDate not supplied

The properdin system: composition and function.

This article summarized the physicohemical data on the factors which compose the properdin system in guinea pig and man. The following other topics are discussed: (1) Activation of the properdin system; (2) Formation of the initiating and amplification C3 convertases; (3) Formation of the C5 convertase, and (4) Regulatory control mechanisms of the properdin system.

Animals↗
PubMed1992

Role of fibrinogen in complement inhibition by streptococcal M protein.

M protein, the major virulence factor of group A streptococci, has antiopsonic activity in that it inhibits activation of the alternative complement pathway on the streptococcal surface. Two properties of M protein have been claimed to account for the inhibitory activity, namely, (i) its binding affinity for complement factor H, which is an inhibitor of alternative pathway activation, and (ii) its high binding affinity for fibrinogen. We have recently shown that fibrinogen, like M protein, inhibits alternative pathway activation by possessing binding affinity for factor H. Here we report that fibrinogen effectively competes with factor H for binding to M protein but retains its own binding affinity for factor H. The presence of fibrinogen did not significantly affect alternative pathway inhibition on the streptococcal surface.

Antigens, Bacterial↗
PubMed1992

Complement activation in neonatal infection.

To investigate the usefulness of indices of complement activation in the diagnosis of infections in the neonatal period, activation products C4d, Ba, and C3d were measured in 42 babies with a putative diagnosis of infection based on clinical/laboratory criteria, and compared with conventional clinical and haematological criteria of infection and with C reactive protein. The diagnosis of sepsis was confirmed by culture and identification of organisms in 17. Fourteen babies in whom infection was not suspected formed the control group. In babies with proved infection, concentrations of the fragments C4d, Ba, and C3d were higher than in babies with suspected infection in whom microbiological tests were negative, and concentrations of Ba and C3d were higher than in controls. C reactive protein and the platelet count were not significantly different in babies with proved infection and those with negative microbiological tests, but in the latter, C reactive protein concentrations were higher than in controls. Of the indices studied, high concentrations of Ba predicted microbiologically proved infection with the highest sensitivity (47.1%) and specificity (92.0%). Ba thus seems to be useful as an early indicator of infection in the neonatal period.

Analysis of Variance↗
PubMed1991

Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin.

Human keratinocytes are able to synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system (CD16, CD36, HLA-DR, intercellular adhesion molecule-1). In the present study, skin biopsies from healthy volunteers, from patients with psoriasis vulgaris (PV), mycosis fungoides (MF), purpura pigmentosa chronica (PPC), acute urticaria (AU) and from positive tuberculin skin tests were investigated with regard to the reactivity with the monoclonal antibodies to complement receptors CR1 CR2 and CR3 by means of a multistep immunoperoxidase method. In the clinically involved skin of all patients with PV, MF or PPC, and in biopsies obtained from positive tuberculin tests, specific epidermal intercellular staining with OKB7 and Leu anti-CR2 was seen on subcorneal keratinocytes. This finding suggests a differentiation-linked expression of CR2 on human keratinocytes in cytokine-mediated skin diseases whereas CR1 and CR3 are apparently not expressed.

Antigens, CD↗
PubMed1977

Human lymphocyte complement receptors. Quantitative requirements for C3 of normal and chronic lymphocyte leukemia lymphocytes.

Erythrocytes coated with varying amounts of human complement were used to detect lymphocytes with complement receptors from normal subjects and patients with chronic lymphocytic leukemia. The relationship between the percentage of lymphocytes rosetting and the quantity of C3 present on complement-coated erythrocytes were studied. Small quantities of C3 (less than 5 fg/erythrocyte) caused maximal rosetting of normal lymphocytes. Maximal rosetting with chronic lymphocytic leukemia lymphocytes was not reached until much greater amounts of C3 were used to coat the erythrocytes. This difference in sensitivity to erythrocyte-bound complement was not due to an increased fraction of complement receptor-bearing cells in the leukemic patients. This loss of sensitivity of the chronic lymphocytic leukemia lymphocyte for complement may play a role in the immune deficiency present in this disease.

Cell Membrane↗
PubMed1992

Pleural SC5b-9 in differential diagnosis of tuberculous, malignant, and other effusions.

A monoclonal antibody against soluble phase-terminal complement complex (SC5b-9) was used to try to differentiate pleural effusions of tuberculous vs malignant and other origin. Effusions of tuberculous origin showed a significantly higher SC5b-9 level than did plasma, suggesting activation of complement in the pleural space. All 26 patients with tuberculous effusions showed SC5b-9 levels in pleural fluid exceeding 2.0 mg/L, while 20 with malignant effusions had levels less than 2.0 mg/L. However, rheumatoid, some parapneumonic, and treated malignant effusions showed SC5b-9 levels above 2.0 mg/L. Considering a value exceeding 2.0 mg/L, the specificity and sensitivity of the SC5b-9 estimation in tuberculosis were 0.74 and 1.0, respectively. The mean values for C4d and Bb fragments of complement were significantly (p < 0.05) higher in the tuberculous than in the malignant effusions. However, the values for Bb in 16 (62 percent) of the 26 patients with tuberculous or malignant effusions were in the same range. The activity of adenosine deaminase (ADA) was higher in the tuberculous than in the malignant effusions. While 18 of 26 patients with tuberculous effusions showed an ADA value exceeding 50 mU/ml, the estimated cutoff point (sensitivity = 0.69), 35 of the 36 nontuberculous effusions showed a true negative value (specificity = 0.97). A correlation between ADA and SC5b-9 values was observed in pleural effusions. These observations suggest that the estimation of SC5b-9 in pleural fluid presents a new approach to differentiating tuberculous vs malignant effusions.

Adenosine Deaminase↗
PubMed1991

Complement fragment C4d and Bb levels in inflammatory skin diseases (e.g. SLE, atopic dermatitis, erythroderma and pustulosis palmaris et plantaris) for assessment of complement activation.

The complement is one of the major effector system in the process of inflammation. Complement activation has been shown to occur in inflammatory dermatoses such as systemic lupus erythematosus, atopic dermatitis, erythroderma of unknown origin, and pustulosis palmaris et plantaris by the elevated blood levels of complement fragments. To clarify the complement activation, especially the alternative pathway involvement, we have measured the concentrations of classical pathway-specific C4d and alternative pathway-derived Bb in the plasma of patients with these inflammatory disorders at a mild to exacerbated stage. Only the SLE plasma showed significantly elevated Bb levels. These results suggest that assessments of plasma C4d and Bb levels may be of value in monitoring the involvement of the complement system in patients with inflammatory dermatoses with significant complement activation.

Adult↗
PubMed1979

Activation of the alternative complement pathway by Torulopsis glabrata.

Torulopsis glabrata is a yeast-like fungus with increasing importance as an opportunistic human pathogen. The role of serum complement in resistance to this infection was studied by chemotactic and opsonic assays. The results indicate that T. glabrata activates complement via the alternative pathway. This may be an important mechanism in host immunity to this fungus.

Candida↗
PubMed1976

A phagocytosis-enhancing factor in human plasma.

A phagocytosis-enhancing factor (PEF) with the capacity to stimulate the ingestion of sensitized sheep erythrocytes by human polymorphonuclear and mononuclear leucocytes has been isolated from human plasma by chromatography on DEAE-cellulose and filtration on Sephadex G-150 and Sephadex G-100. PEF is a protein of approximately 70,000 molecular weight which is susceptible to inactivation by heating at 60 degrees or by tryptic digestion. PEF promotes phagocytosis of erythrocytes sensitized with intact 7S antibody or bearing the C3b complement fragment, but not of unsensitized erythrocytes or erythrocytes sensitized with 19S antibody. The specificity of PEF interaction with target erythrocytes and the persistence of its stimulatory effect after the target cells are washed suggest that it promotes phagocytosis by an action on the erythrocytes.

Antibodies↗
PubMed1992

[Recent advances in xenotransplantation].

Interest in xenotransplantation has dramatically increased in the past 4 years, focusing on the potential use as donors of distantly related animals such as pigs (discordant xenografts). The major barrier is hyperacute rejection. The mechanisms responsible for this rejection include: specific reaction of the recipient's natural antibodies with antigens in the donor's organ, direct activation of the recipient's complement system by endothelial cells in the donor's organ, and/or relative failure of complement inhibitory proteins in the donor's organ to impede activation of the recipient's complement system. In case of vascularized xenograft, the temporary depletion of anti-donor antibodies (anti-ABH or anti-HLA class I) from a graft recipient may allow the long term survival of the graft despite a possible return of the antibodies to the circulation. This phenomenon is called accommodation. The mechanisms involved could be: the endothelial cells in a graft develop a resistance to complement mediated injury; the antigens expressed on the blood vessels become modulated or changed; the natural antibody repertoire changes in such a way that there are fewer anti-donor antibodies. The accommodation phenomenon encourages the view that the barrier to xenotransplantation is not immutable.

Complement C3b↗