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PubMed1985

Differences in susceptibility to infection with Treponema pallidum (Nichols) between five strains of guinea pig.

Groups of 10 young male guinea pigs of inbred strains 2 and 13 and outbred strains Hartley A, Hartley B, and one deficient in the fourth component of complement (C4D) were infected intradermally with 80 X 10(6) Treponema pallidum (Nichols). The course of infection and production of antitreponemal antibody were examined. Strain C4D guinea pigs were the most susceptible to infection (100%); inbred strains 2 and 13 and outbred strain Hartley B showed 80-90% symptomatic infection; and the Hartley A strain was the least susceptible to infection (10%). Strain 13 animals responded with the highest antitreponemal antibody activity, and the Hartley A strain with the lowest. The results suggest that genetic factors or complement, or both, may influence the degree of susceptibility to infection with T pallidum in guinea pigs.

Animals↗
PubMed1986

I (C3b/C4b inactivator) typing by agarose gel isoelectric focusing and immunoblotting technique.

Genetic polymorphism of I (C3b/C4b inactivator) was studied by the method of agarose gel isoelectric focusing followed by an immunoblotting technique. Serum or plasma samples were pretreated with neuraminidase. The method is rapid, and gives the simple and reliable patterns of I. The allele frequencies calculated from healthy Japanese individuals living in the western part of Japan were: IF* A = 0.126 and IF*B = 0.874.

Blood Proteins↗
PubMed1987

Genetic markers in patients with intracranial aneurysms.

HLA antigens, blood group systems (ABO, Rh, MNSs, P, Kell, Lewis and Duffy) and serum group systems (Hp, Tf, Gc, Pi, Bf, C3 and C4) were studied in a series of patients with intracranial aneurysms. A significantly increased frequency of HLA antigen A28, a significantly decreased frequency of HLA antigen B40, and a significantly decreased frequency of complement factor C4 B2 was found among the patients when compared with controls from the same geographic area.

Complement C4↗
PubMed1989

Glomerular deposition of C4 cleavage fragment (C4d) and C4-binding protein in idiopathic membranous glomerulonephritis.

Renal biopsies from 12 patients with idiopathic membranous glomerulonephritis (IMGN) were investigated by immunofluorescence microscopy for the localization of C4d and C4-binding protein (C4bp). Although Clq and C4 deposits were found in only 2 of 12 cases (16%), C4d and C4bp deposits were identified in 11 cases (92%) in close association with IgG deposits in the glomeruli. The results suggest that complement activation through the classical pathway usually occurs in IMGN. The detection of C4d and C4bp in the glomeruli appears to be a sensitive indicator of the classical pathway activation in IMGN.

Carrier Proteins↗
PubMed1984

Studies on the binding of complement factor C4 in human platelets. Complement activation by means of cold agglutinins.

Normal human platelets were investigated by immunofluorescence techniques for the natural occurrence of and uptake capacity for complement factor C4. Fractions of human platelets were found to carry none or very little C4. Activated C4 was readily taken up by the majority of platelets in vitro. Complement could be activated with pathological cold agglutinins (CA) of mono- or polyclonal types, all with specificity for the I antigen. Complement activation seen in normal human sera was probably due to naturally occurring CA with anti-I specificity. Thrombin potentiated the complement-activating capacity of CA, and complement factor C1 enhanced and stabilized the binding of CA to platelets.

Agglutinins↗
PubMed1989

Assessment of the activation pathways of the complement in psoriatic patients by use of complement fragment C4d and Bb measurements.

We have measured the complement fragment C4d and Bb levels in the plasma of 51 psoriatic patients and 54 normal controls. The C4d and Bb levels were not significantly elevated in the plasma of the psoriatic patients when compared with those of controls, except in patients with more than 60% skin involvement who exhibited an increase in Bb levels. C4d levels, however, did decrease slightly after successful treatment of psoriasis. Although these results suggest that the C4d and Bb levels partly reflect the complement activation in vivo, they do not seem to be suitable parameters to clarify the mechanism of complement activation in psoriasis.

Adolescent↗
PubMed1991

Sarcoidosis and major histocompatibility complex genes with special emphasis on BF F subtypes.

Frequencies for HLA class I and II histoglobulins and C4A, C4B, BF complement proteins were performed for 59 sarcoidosis patients. The DR5 allele was present in 55.9% of patients as compared to 31.5% of controls. We noticed that its increase was more relevant in males and in those with a poor prognosis. BF F allele was significantly over-represented in patients (29.09% vs. 19.15% of control), especially in women. Special emphasis was given to BF F subtyping, to define an association between a particular BF F subtype and patient's sex or disease outcome.

Alleles↗
PubMed1985

Immunoelectrophoretic analysis of C4 split products expressing D but not C epitopes: influence of storage, Ca2+ and Ca2+-chelating agents.

Based on immunoelectrophoretic methods a heterogeneity in the electrophoretic mobility of C4d was observed. C4d was defined immunochemically as C4 molecules expressing D but lacking C epitopes. A beta-mobile form was observed when EDTA or heparin was not added to the sample prior to electrophoretic analysis. This component was generated during electrophoresis. Another C4d component migrating to the post-albumin region probably represented an in vivo generated split product. However, this C4d form was also produced during storage of serum or plasma at room temperature and its formation was enhanced in the presence of EDTA. Based on these findings standard conditions for collection and storage of clinical samples for quantification of C4d by electroimmunoassay are suggested.

Calcium↗
PubMed1996

Blood protein interactions with titanium surfaces.

Protein adsorption and complement activation were studied on thin evaporated films of titanium (Ti). The surfaces were cleaned in either a radio frequency (RF) plasma unit, or washed sequentially in trichloroethylene, acetone, ethanol, and water. Both methods resulted in hydrophilic surface with low carbon contamination on the outermost oxide (approximately 11-13 at%). In situ ellipsometry suggested that Ti is an intrinsic coagulation activator in vitro, since significant amounts of factor XII (F XII) and high molecular weight kininogen (HMWK) were found on the surfaces after 1 min incubation in heparin plasma. Ellipsometry, performed after serum incubations ranging from 15 s to 30 min showed that the total amount of serum proteins and the deposition of antibodies to complement factor 3c (C3c) increased with serum incubation time. ELISA methods showed increased levels of free iC3b in serum after 10 min incubation of the surfaces, but no detectable amounts of C3 convertase fractions C4d or Bb. Ellipsometric results indicated, however, an increased deposition of antibodies to CIq and IgG on Ti after short serum incubation times. The combined results indicate that Ti-surfaces initially activate complement through the classical pathway. The activation then continues via a positive amplification loop where increased amounts of C3 are deposited on the surfaces via the alternative pathway.

Acetone↗
PubMed1996

Blood protein interactions with chromium surfaces.

Protein adsorption, contact activation, and complement activation were studied on thin evaporated films of chromium (Cr) in vitro. The surfaces were, prior to the experiments, cleaned in either ethanol and water, or in a basic peroxide solution (RCA standard clean 1, SC-1). Surface spectroscopic studies of the outermost oxides showed a significant reduction of carbon contaminants after washing in SC-1 but also suggested an increase in the oxidation state as compared with the ethanol-washed surfaces. In situ ellipsometry combined with antibody techniques was used to determine protein deposition and antibody binding onto surfaces after incubations in heparin plasma or in normal serum. Incubation times from 1 to 10 min in serum showed increased depositions of serum and antibodies to complement factor 3c (C3c) and was larger on ethanol-washed surfaces than on surfaces washed in SC-1. ELISA methods indicated increased amounts of iC3b in serum for both surfaces, but no presence of C3 convertases (C4d or Bb fractions). A low or transient complement activation via the classical pathway was indicated on ethanol washed Cr, since deposition of secondary antibodies to complement factor Iq (CIq) was observed only after short incubation times in serum. No procoagulant activity of Cr was indicated, since only low amounts of antibodies to factor XII (F XII), prekallikrein (PKK), and high molecular weight kiniogen (HMWK) bound to the surfaces after incubations in heparin plasma. These results were confirmed using a colorimetric assay where the relative amounts of free plasma kallikrein was assessed using a chromogenic substrate, H-D-Pro-Phe-Arg-pNA (S-2302).

Adsorption↗
PubMed1991

Leukocyte adhesion-deficient neutrophils fail to amplify phagocytic function in response to stimulation. Evidence for CD11b/CD18-dependent and -independent mechanisms of phagocytosis.

Stimulation of PMN with inflammatory mediators markedly augments Fc and CR1 receptor-mediated ingestion. However, CD11/CD18-deficient PMN from three patients with complete leukocyte adhesion deficiency (LAD) failed to recruit phagocytic function in response to phorbol esters, cytokine, or Arg-Gly-Asp-containing ligand stimulation. Because stimulated ingestion is protein kinase C (PKC)-dependent, our data indicate that LAD PMN exhibit only PKC-independent phagocytosis. The defect in PKC-dependent ingestion is specific for CD11b/CD18 and not secondary to the chronic or recurrent infections which occur in this disease. The LAD phenotype for phagocytic function can be reproduced in normal PMN by the anti-CD11b MAbs OKM1 and OKM10. In contrast, MAb Mo1 (anti-CD11b) and MAb IB4 (anti-CD18) inhibit both CD11b/CD18-dependent and -independent mechanisms of ingestion by normal PMN. Their ability to inhibit CD11b/CD18-independent ingestion may be mediated by cAMP, as shown by experiments with a protein kinase A inhibitor HA1004 and by direct measurement of cAMP levels in immune complex- and FMLP-stimulated PMN. These data indicate that CD11b/CD18-independent and -dependent mechanisms of phagocytosis exist and that some effects of anti-CD11b/CD18 MAbs may be mediated by alterations in cAMP levels.

Antibodies, Monoclonal↗
PubMed1997

Effect of beta 2glycoprotein I and human monoclonal anticardiolipin antibody on the protein S/C4b-binding protein system.

The effect of beta 2glycoprotein I (beta 2GPI) and human monoclonal anticardiolipin antibody (aCL) on the protein S/C4b-binding protein (C4BP) system was evaluated. The binding of C4BP to protein S was assessed by ELISA in the presence of beta 2GPI with/without human monoclonal aCL. beta 2GPI downregulated the binding between S and C4BP significantly. Human monoclonal aCL abolished the beta 2GPI inhibitory effect in a calcium (Ca++) independent fashion. In separate experiments, the reactivity of aCL towards protein S in the presence or absence of beta 2GPI and cardiolipin was investigated. Monoclonal aCL bound to protein S only in the presence of a combination of beta 2GPI and cardiolipin. This binding was Ca++ dependent. These findings suggest that human monoclonal aCL increases the affinity of C4BP for protein S, and that protein S may represent one of the targets for aCL when combined with beta 2GPI and cardiolipin. Both issues may explain acquired free protein S deficiency and the attendant risk of thrombosis in patients with aCL.

Animals↗
PubMed1986

Different patterns of C3 and C4 activation in the varied types of juvenile arthritis.

Quantitative assays for C3 and C4 activation were carried out simultaneously on blood from children with varied types of juvenile arthritis. Factor VIII-related antigen was also measured as an indicator of vascular damage. In active systemic juvenile arthritis, the C4d/C4 ratio was frequently elevated and was usually associated with elevated C3d/C3 ratios and elevated concentrations of factor VIII-related antigen. Children with chronic polyarticular arthritis, no matter which forms of onset they had had, also had increased levels of the C4d/C4 ratio, C3d/C3 ratio, and factor VIII-related antigen, but these were less consistent and were not associated with each other. In contrast, in pauciarticular arthritis there was a uniquely isolated increase in the C3d/C3 ratio. This work implies that there are different mechanisms responsible for complement activation in the different types and at different stages of juvenile arthritis.

Adolescent↗
PubMed1990

A case of first trimester prenatal diagnosis of 21-hydroxylase deficiency with human complement C4 cDNA probe.

Early prenatal diagnosis of 21-hydroxylase (21-OHase) deficiency would enable treatment to be done to protect the fetus from masculinization and/or life-threatening adrenal crisis at birth. We report here the prenatal diagnosis of 21-OHase deficiency with human complement component C4 cDNA to probe DNA from chorionic villi at 10 weeks of gestation. Southern analysis with human C4 cDNA identified TaqI restriction fragment length polymorphisms (RFLPs) in the family. Family analysis with these RELPs showed that the fetus was not affected at greater than 99% probability, because the frequency of recombination between the 21-OHase B gene and the C4 gene would be extremely low.

Adrenal Hyperplasia, Congenital↗
PubMed1990

HLA class I-, complement C4- and 21-hydroxylase probes in the genetic analysis of 21-hydroxylase deficiency.

In order to develop an optimal strategy for the prenatal diagnosis of steroid 21-hydroxylase (EC 1.14.99.10) deficiency, we investigated 16 affected families with salt wasting syndrome. Genomic DNA derived from peripheral white blood cells was digested with 6 different restriction enzymes. Hybridisation was carried out with DNA-probes of the HLA class I region, the 21-hydroxylase- and the complement C4 genes. All the families were informative in at least three different loci. Twelve out of the 16 families were informative by neutral polymorphisms or disease related variants of the 21-hydroxylase gene or the adjoining C4 locus. The reliability of prediction in these cases exceeded 99%. The remaining 4 families were informative only in the HLA class I region, tantamount to a reliability of prediction of about 98%. In none of the cases did we have to fall back on semiquantitative gene dose assessments. We further describe new polymorphisms in the 21-hydroxylase region for the enzyme Pvu II and EcoR V.

Adolescent↗
PubMed2001

Chronic humoral rejection: identification of antibody-mediated chronic renal allograft rejection by C4d deposits in peritubular capillaries.

The pathogenesis of chronic renal allograft rejection (CR) remains obscure. The hypothesis that a subset of CR is mediated by antidonor antibody was tested by determining whether C4d is deposited in peritubular capillaries (PTC) and whether it correlates with circulating antidonor antibodies. All cases (from January 1, 1990, to July 31, 1999) that met histologic criteria for CR and had frozen tissue (28 biopsies, 10 nephrectomies) were included. Controls were renal allograft biopsies with chronic cyclosporine toxicity (n = 21) or nonspecific interstitial fibrosis (n = 10), and native kidneys with end-stage renal disease (n = 10) or chronic interstitial fibrosis (n = 5). Frozen sections were stained by two-color immunofluorescence for C4d, type IV collagen and Ulex europaeus agglutinin I. Antidonor HLA antibody was sought by panel-reactive antibody analysis and/or donor cross matching in sera within 7 wk of biopsy. Overall, 23 of 38 CR cases (61%) had PTC staining for C4d, compared with 1 of 46 (2%) of controls (P < 0.001). C4d in PTC was localized at the interface of endothelium and basement membrane. Most of the C4d-positive CR tested had antidonor HLA antibody (15 of 17; 88%); none of the C4d-negative CR tested (0 of 8) had antidonor antibody (P < 0.0002). The histology of C4d-positive CR was similar to C4d-negative CR, and 1-yr graft survival rates were 62% and 25%, respectively (P = 0.05). Since August 1998, five of six C4d-positive CR cases have been treated with mycophenolate mofetil +/- tacrolimus with a 100% 1-yr graft survival, versus 40% before August 1998 (P < 0.03). These data support the hypothesis that a substantial fraction of CR is mediated by antibody (immunologically active). C4d can be used to separate this group of CR from the nonspecific category of chronic allograft nephropathy and may have the potential to guide successful therapeutic intervention.

Adult↗
PubMed1992

Histocompatibility antigens associated with Behçet's disease in northern Han Chinese.

Among Han nationality Chinese and living in the northern area of the Yellow River, 120 patients suffering from Behçet's disease and 100 unrelated healthy individuals were typed for histocompatibility antigens (HLA)-A, -B, -C, and -DR and -DQ antigens. HLA-DR and DQ typing was performed on B-lymphocyte separated with Lympho-B-Kwik. The HLA-antisera were provided by 11th IHWC. Bf alleles and C4 allotypes were determined by immunofixation agarose-gel electrophoresis. HLA-B51 was found in 67/120 (55.83%) patients and in 12/100 (12%) controls, the Chi-square and relative risk values were 45.54 and 9.27, respectively (p < 0.0005). C4AQ0 frequency was significantly increased in the patient group. In the complete form group HLA-B51 was observed more frequently (62.79%). No significant differences of other HLA antigens, frequencies, Bf or B4 alleles were found between the groups.

Adult↗
PubMed1996

Restriction fragment length polymorphism analysis in the HLA class III genes of patients with diffuse panbronchiolitis.

Although diffuse panbronchiolitis (DPB) is known to be positively associated with certain major histocompatibility complex (MHC) class I antigens, e.g., HLA-B54 in Japanese patients, it is not clear whether the MHC genes predispose to the disease or are markers for other disease susceptibility gene(s). Because the HLA class III genes such as tumor necrosis factor (TNF) or the fourth component of complement (C4) are localized in the proximity of the HLA-B locus, one or more of these genes might be responsible for susceptibility to DPB. To analyze the role of HLA class III genes in DPB patients, we first evaluated the HLA-B54 association in 32 patients with DPB, and subsequently, studied the restriction fragment length polymorphism (RFLP) of the TNF-alpha and -beta (TNF-alpha/beta) genes as well as the C4A and B (C4A/B) genes in DPB patients and normal individuals. The HLA-B54 antigen was significantly more frequent in DPB patients than in normal individuals (40.3% vs 13.0%, p < 0.001), however, we did not detect a significant association between DPB and gene polymorphisms of either TNF-alpha/beta or C4A/B. Furthermore, there was no evidence of C4A gene deletion in patients with DPB. These results suggest that the HLA-B54 antigen itself might be directly involved in the pathogenesis of DPB.

Bronchiolitis↗