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PubMed1984

Silent lupus nephritis among patients with discoid lupus erythematosus.

A kidney biopsy was performed in 7 hypocomplementemic discoid lupus erythematosus patients despite the absence of overt renal involvement. Five patients had glomerular immune deposits and 2 patients with disseminated discoid lupus erythematosus exhibited definite proliferative glomerulonephritis. Those findings show that silent lupus nephritis may be encountered in discoid as well as in systemic lupus erythematosus, providing additional evidence supporting the unity of the disease. We suggest that hypocomplementemic patients with discoid lupus erythematosus must be carefully screened for renal disease by periodic urinalysis examinations.

Complement C3↗
PubMed1983

[Extramembranous glomerulonephritis of acquired syphilis in a patient recently infected by the hepatitis B virus. Demonstration of the treponemal antigen in the kidney by indirect immunofluorescence].

A 38 years old male homosexual with active secondary syphilis presented with pure nephrotic syndrome while HBs and HBe tests were positive without clinical hepatitis. He had circulating immune complexes, IgG--IgM cryoglobulinemia and high IgA, IgM and IgE levels; the C3 and C4 complement constituents were normal. Examination of renal biopsy sections under light, fluorescent and electronic microscopy showed stage I membranous glomerulonephritis the syphilitic origin of which was confirmed by indirect immunofluorescence and by rapid cure under penicillin treatment. This case calls for the following comments: (1) glomerular deposits are extramembranous rather than subendothelial in syphilitic nephrosis, a disease now classified among circulating immune complexes diseases; (2) in the kidney, the treponema antigen can be demonstrated by indirect immunofluorescence and the anti-treponema antibody, by elution; (3) the outcome of the nephrotic syndrome is always favourable, either spontaneously or after penicillin treatment; (4) syphilis and HBs antigens are frequently associated, particularly in homosexual patients; one should be looked for when the other is discovered.

Adult↗
PubMed1984

Structure and function of the human C3b receptor.

The human C3b receptor (C3bR) is a glycoprotein that exists in two allotypic forms having Mr values of approximately 250,000 (F) and 260,000 (S). The number of receptors present on erythrocytes varies by eightfold among normal individuals and is genetically regulated by two codominant alleles that are distinct from the alleles determining the structural polymorphism. C5a and C5ades Arg induce rapid increases in the number of receptors expressed by neutrophils in vitro, and probably account for the increased receptor expression on neutrophils in patients undergoing hemodialysis. Cytoskeletal association of the C3bR on monocytes and neutrophils is suggested by experiments demonstrating receptor-mediated phagocytosis and adsorptive endocytosis through coated pits, and by the reciprocal coredistribution of cross-linked C3b and Fc receptors and the detergent insolubility of cross-linked C3bR. The factor H-like cofactor activity of the C3bR promotes the cleavage of bound C3b to iC3b, C3c, and C3d,g, which may enhance the clearance of circulating immune complexes and the generation of ligands for CR2 and CR3. The inherited partial deficiency of the erythrocyte C3bR in patients with systemic lupus erythematosus and the absence of glomerular C3bR in these patients with proliferative glomerulonephritis may contribute to systemic and organ-specific abnormalities in the clearance of immune complexes in this disease.

Complement C4↗
PubMed1984

C3-independent immune haemolysis: haemolysis of EAC14oxy2 cells by C5-C9 without participation of C3.

C3-independent immune haemolysis was studied using EAC14oxy2 cells and purified C5, C6, C7, C8 and C9. We have found that EAC14oxy2 cells were lysed by C5-C9 and that haemolysis occurs, even after pretreatment of the cells and the C5-C9 preparation with anti-C3. This indicates that EAC14oxy2 can be lysed by C5-C9 without any participation of C3. In contrast, EAC1 and EAC14 cells are not lysed by C5-C9, suggesting that our C5-C9 preparation lacks activated complement components, such as C3bBb, C5b6 or C(56)a. Based on our study of the haemolysis of EAC14oxy2, we have determined that: (i) EAC14oxy2 cells are lysed by a preparation of C5, C6, C7, C8 and C9, but no lysis occurs when any one of these complement is absent, (ii) for significant haemolysis of EAC14oxy2, a higher concentration of C5 is necessary as compared to the C5 requirement when haemolysis occurs in the presence of C3, (iii) the degree of haemolysis is linearly related to the concentration of C5 and does not reach a plateau, despite the addition of as much as 3,200 U of C5, and (iv) the degree of haemolysis is linearly related to the concentration of cell bound C42. These observations suggest that, in the absence of C3, the C3 convertase C42 can activate C5 directly, resulting in the formation of the membrane attack complex, C5b-9.

Complement C2↗
PubMed1982

Antibody, immune complexes, and complement activity fluctuations in kittens with experimentally induced feline infectious peritonitis.

Humoral changes were studied in 6 specific-pathogen-free kittens during experimental infection with feline infectious peritonitis virus. Although the incubation period and the duration of the disease differed widely, a similar pattern of rectal temperatures, serum complement values, circulating immune complexes, and antibody titers was found for all kittens during the last 15 to 20 days of life. Antibody formation started 8 to 13 days before death and was accompanied by the appearance of circulating immune complexes with subsequent increased concentrations of complement followed by complement depletion. The data are discussed as evidence for an immune complex pathogenesis of feline infectious peritonitis.

Animals↗
PubMed1984

Generation of the classical pathway C3 convertase (EAC4b2a) by proteolytic enzymes.

The formation of EAC 4b2a is a two step reaction: first, the temperature- and time-independent binding of C2 to EAC4b2a resulting in EAC4b2 , secondly, the enzymatically triggered conversion of EAC4b2 to EAC4b2a . In the classical cascade of complement activation, the generation of C3 convertase activity is triggered by the C1 esterase, C1-s, which is part of C-1. Evidence is presented that the enzymes trypsin, chymotrypsin, plasmin, and pronase are also able to activate EAC4b2 to EAC4b2a . Kinetic studies showed that the formation of C3 convertase by these enzymes was dependent on concentration, temperature, and time. The optimal conditions were found as follows: trypsin, 2 micrograms/ml (final conc.) for 8 min at 23 degrees C; chymotrypsin 165 micrograms/ml for 18 min at 23 degrees C; plasmin 0.8 units/ml for 15 min at 23 degrees C; pronase 1.25 microgram/ml for 15 min at 23 degrees C. Even under optimal (tmax) conditions the number of generated EAC4b2a differed from enzyme to enzyme: trypsin (= 100%), pronase (58.3%), chymotrypsin (47.9%), and plasmin (12.9%). The enzymes were also able to generate C3 convertase activity from C2 which was adsorbed to EAC1i4b , a C1 inactivator treated and therefore hemolytically inactive intermediate ( EAC1i4b2 ). These findings underline the biological importance of C1 esterase replacing enzymes.

Animals↗
PubMed1984

[The anticomplementary activity of 2 intravenous gamma globulin preparations in children with acute lymphatic leukemia].

Children with acute lymphocytic leukemia received gammaglobulin replacement therapy using either one of two i.v. gammaglobulin preparations in order to reduce the frequency and severity of infections during cytostatic treatment. Sera and EDTA-plasma taken prior to each infusion and following each infusion were analyzed for several complement components and immune complexes in order to assess in vivo anticomplementary activity. Preliminary data published in this paper show only little changes in the complement system. This may be related to fact that infusions were well tolerated. IgG-levels could be raised for more than 200 mg/dl by administration of doses around 150 mg/kg body weight.

Adolescent↗
PubMed1980

Control of serum C3 levels by beta 1H and C3b inactivator.

In serum specimens from 50 normal adults, a high correlation was found between the sum of the levels of the control proteins of the C3b amplification loop, C3b inactivator and beta 1H, and the sum of the component proteins, C3 and factor B (R = 0.83), when the concentrations are expressed as percent of the normal adult level. The slope for this regression was 0.98 and the y intercept practically zero, indicating that under normal conditions, beta 1H + C3b inactivator = C3 + factor B +/- 35% (95% error of the prediction). Biological significance of the combined values was suggested by the fact that their equality was largely preserved in serum specimens from cord blood, from infants, and from patients with idiopathic nephrotic syndrome, malnutrition, chronic illness, and partial C3b inactivator deficiency even though, individually, control and component protein concentrations deviated from normal in many of these conditions and, as single proteins, did not correlate with each other as in normal subjects. On the other hand, C3 + factor B was disproportionately lower than beta 1H + C3b inactivator in subjects heterozygously deficient in C3 and in those with hypocomplementemic glomerulonephritis and was often disproportionately high in those with an acute-phase reaction. The data indicate that for meaningful interpretation of the serum C3 level, the concurrent levels of factor B, C3b inactivator, and beta 1H must be taken into consideration.

Adolescent↗
PubMed1984

Serial determination of complement and specific antibody titres in Pseudomonas aeruginosa infection.

Serial examination of the complement system and specific antibody titre of 12 surviving patients and 8 lethal cases suffering from Pseudomonas aeruginosa infection showed that except the onset of infection, until the development of septic shock, the level of the complement components corresponded to or exceeded the average normal value. In reversible septic shock the complement titre decreased significantly and in irreversible shock the values were even lower. Activation of the complement system occurred on 10 occasions via the classical and on 42 occasions via the alternative pathway. The number of activations grew parallel with the severity of the infection. Activation through the classical way was generally more intensive. During the whole infectious process not the individual characteristics of the P. aeruginosa present unbroken, but the pathological events and the specific antibody level determined the mode (alternative or classical pathway) of complement activation. The specific antibody level of the surviving patients significantly surpassed the titres of the lethal cases until the development of shock. Not an insufficiency of the complement system but the relative lack of specific antibodies was mainly responsible for the fatal outcome of P. aeruginosa infections.

Antibodies, Bacterial↗
PubMed1984

Recurrent meningococcal meningitis. A case report.

A 17-year-old Coloured youth presented at Tygerberg Hospital on six occasions between 1978 and 1981. He was admitted three times for meningococcal meningitis and three times for a meningitic illness clinically suggestive thereof. He had been admitted twice before to the City Hospital, Cape Town, in 1966 and 1968, for presumed meningococcal meningitis. He was fully evaluated in the outpatient department and found to have no detectable total haemolytic complement activity. There was no evidence of classic or alternative pathway activation. He has been tentatively designated as having a deficiency in the C6 or C8 components of the terminal membrane attack mechanism of the complement cascade.

Adolescent↗