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PubMed1998

[Soluble tumor necrosis factor receptors in patients with systemic lupus erythematosus].

OBJECTIVE: To study the variations of type II soluble receptors for tumor necrosis factor (sR-TNF) in patients with systemic lupus erythematosus and investigate their use in the clinical setting. PATIENTS AND METHODS: Twenty-six patients with systemic lupus were followed for a mean 3 years. sR-TNF and other immunological parameters (C reactive protein, anti-DNA antibodies, C3 and C4 complement fractions, soluble receptors for interleukin 2) were measured in sera at different points of the disease course. The systemic lupus activity measure (SLAM) was determined at each point, and confronted with the biology results. The study was cross sectional for the group and longitudinal for the patients. RESULTS: sR-TNF was the immunological parameter which correlated best with SLAM. It also correlated with sedimentation rate, C reactive protein, thrombopenia, anemia, creatinine level, anti-DNA antibodies and sR-IL2. The longitudinal study pointed out however that this finding is not consistent for each patient. CONCLUSION: A rise in sR-TNF related to systemic lupus activity but is of limited practical interest for individual patient follow-up.

C-Reactive Protein↗
PubMed1976

Detection and characterization of circulating immune complexes in rheumatoid arthritis.

Circulating immune complexes (IC) were detected and quantified in serum of patients with rheumatoid arthritis (RA) by three methods: radiolabeled Clq binding test, anticomplementary activity and optical density of 3% PEG precipitated sera. Rheumatoid factor (RF) is characterized in PEG precipitates by the Waaler-Rose reaction. The relationship between IC, complement and RF levels are analyzed.

Antigen-Antibody Complex↗
PubMed1994

Selective expression of clusterin (SGP-2) and complement C1qB and C4 during responses to neurotoxins in vivo and in vitro.

This study concerns expression of the genes encoding three multifunctional proteins: clusterin and two complement cascade components, C1q and C4. Previous work from this and other laboratories has established that clusterin, Clq and C4 messenger RNAs are elevated during Alzheimer's disease, and in response to deafferenting and excitotoxic brain lesion. This study addresses hippocampal clusterin, ClqB and C4 expression in response to neurotoxins that caused selective neuron death. Kainate, which preferentially kills hippocampal CA3 pyramidal neurons but not dentate gyrus granule neurons induced clusterin immunoreactivity in CA1 and CA3 pyramidal neurons and adjacent astrocytes, but not in dentate gyrus granule neurons. In contrast, colchicine, which preferentially kills the dentate gyrus granule neurons, induced clusterin immunoreactivity in the local neuropil as punctate deposits, but not in the surviving or degenerating dentate gyrus granule neurons. Clusterin messenger RNA was increased in astrocytes. ClqB and C4 messenger RNAs increased within 48 h after kainate injections, particularly in the CA3 pyramidal layer, less in the dentate gyrus-CA4, and less in CA1. Clq immunoreactivity was detected in CA1 pyramidal neurons and also as small punctate deposits in the CA1 region at eight and 14 days after kainate. The increase of both clusterin and ClqB messenger RNAs after kainate injections was blocked by barbiturates that prevented seizures and neurodegeneration. In primary hippocampal neuronal cultures treated with glutamate, a subpopulation of cultured neurons that survived glutamate toxicity also had parallel elevations of clusterin and ClqB messenger RNA. In conclusion, cytotoxins that target selective hippocampal neurons increase the expression of both clusterin and ClqB in vivo and in vitro. These results show that elevations of clusterin messenger RNA or protein can be dissociated from each other and from cell death. These increased messenger RNAs were associated with immunoreactive deposits that differed by cell type and intra- versus extracellular locations. These results suggest that the complement system is involved in brain responses to injury.

Animals↗
PubMed1996

Serum angiotensin converting enzyme and C4 protein of complement as a combined diagnostic index in alcoholic liver disease.

Diagnosis of liver cirrhosis relies on hepatic biopsy. So far, attempts have failed to achieve a serologic test that differentiates cirrhosis from other hepatic conditions. The aim of this work was to assess the diagnostic value of the ratio of serum angiotensin converting enzyme activity (SACE) and the levels of protein C4 of serum complement (SACE/C4) in differentiating cirrhotic from noncirrhotic alcoholic liver diseases. In this study, 68 active alcoholic patients (17 with fatty liver or minimal changes, 11 with acute alcoholic hepatitis and 40 with cirrhosis) were included. Twenty healthy subjects were studied as a control group. Liver biopsy was performed in all patients. SACE levels were significantly higher in the group with cirrhosis when compared with the group of patients without cirrhosis and the control. On the other hand, serum C4 level decreased as liver damage progressed. SACE values above 25 IU/l had a sensitivity of 92.5 percent (95 percent confidence interval, 87.5 to 97.5) and a specificity of 79 percent (95% percent confidence interval, 70.5 to 87.5), in detecting those patients with liver cirrhosis. The sensitivity further increased to 95 percent (95 percent confidence interval, 90.5 to 99.5) and the specificity to 100 percent when the SACE/C4 ratio was used and a cutoff point of 145 was chosen. To conclude, in alcoholics SACE is specifically elevated in patients with cirrhosis, and the SACE/C4 ratio is a excellent biochemical index for the diagnosis of cirrhosis in alcoholic patients.

Adult↗
PubMed1986

Guinea pigs with inherited deficiencies of complement components C2 or C4 have characteristics of immune complex disease.

Guinea pigs genetically deficient in the second (C2) or fourth component of complement (C4) generally appear healthy in contrast to humans with a C2 or C4 deficiency. However, upon investigation of these genetic deficiencies in guinea pigs for signs of dysregulation in the humoral immune system and especially autoantibodies, many complement-deficient guinea pigs (greater than 50%) had elevated levels of serum IgM and higher concentrations of anti-hapten (dinitrophenyl) antibodies as signs of polyclonally stimulated antibody synthesis. In addition, a significant number of the complement-deficient animals, on average 30%, had IgM rheumatoid factors in their sera compared with less than 1% of the normal animals. These observations, therefore, indicate that guinea pigs, genetically deficient in C2 or C4, show characteristics of immune complex disease in general.

Aging↗
PubMed1981

Rocket immunoelectrophoresis of C4 and C4d. A simple sensitive method for detecting complement activation in plasma.

Activation of complement component C4 has recently been measured by the quantitation of C4 and C4d (a cleavage fragment of C4) by electroimmunodiffusion in gels containing specific precipitating antibodies for C4 and C4d (Rocket immunoelectrophoresis, RIE). Quantitative measurements of the complement component C4 and its fragment C4d were determined in rocket immunoelectrophoresis (RIE) and compared with measurements of total hemolytic complement activity (CH50) or concentrations of C4 as determined by single radial immunodiffusion (RID). This newly developed RIE assay shows activation of the classical complement pathway and involves electroimmunodiffusion in gels containing specific precipitating antibodies for C4 and its cleavage fragment, C4d. In 37 plasma samples, excellent correlation was demonstrated between the C4 in RIE and CH50 (r = .70) and C4 by RID (r = .87). In vivo activation of C4 was determined by measuring the ratio of C4d to C4; 21 of the plasma samples assayed had ratios greater than 1.1 indicating activation of C4. In 13 of the plasma samples there were correspondingly low CH50 values, whereas 8 had normal CH50 levels. Therefore, activation can be detected in those instances when other measurements (CH50 and C4 quantitation) are normal. Thus the RIE assay for plasma C4 activation appears to be the most sensitive method available for assessing in vivo activation of the classical pathway of complement.

Animals↗
PubMed2003

[Complement split product C4 as the indicator of immunological activity in chronic allograft rejection].

The patients after renal transplantation with deteriorating graft function were included to the study. The aim of the study was to establish the usefulness of stabile complement split product C4d expression as the independent indicator of immunological activity in chronic rejection. The C4d expression was studied on fresh frozen tissue with immunofluorescence method. The intensification of immunosuppression regimen was also introduced and azathioprine was exchanged with mycofenolate mofetil. The protocol biopsies a year after inclusion are planned to be done. In our study there was positive correlation between C4d expression and previous acute rejection episodes, morphological changes specific for chronic rejection and clinical improvement after immunosuppression enhancement.

Adult↗
PubMed2005

Effects of C-reactive protein and the third and fourth components of complement (C3 and C4) on incidence of atrial fibrillation.

Although C-reactive protein (CRP) is a major cardiovascular risk factor, its association with atrial fibrillation (AF) remains controversial. This study explored whether the CRP-related incidence of AF is modified by serum markers of inflammation in a population-based cohort with follow-up data. Serum CRP and 2 components of the complement system (C3 and C4) were determined in 1,011 healthy patients (25 to 64 years old). The incidence of AF was compared between groups defined by levels of CRP, C3, and C4. The follow-up time was 4 years. A high complement level was defined as either C3 or C4 in the top quartile. High CRP was associated with high complement components. An increased CRP level was associated with an increased incidence of AF. The complement components modified these associations. After risk factor adjustment, those with high CRP and high complement components had a significantly higher risk of AF (relative risk 3.0, 95% confidence interval 2.0 to 4.2) than those with normal CRP and low complement levels. In the absence of a high complement level, a high CRP level was not significantly associated with AF (relative risk 1.1, 95% confidence interval 1.0 to 1.4). In conclusion, high CRP levels are associated with high serum levels of complement components. These proteins increase the CRP-related incidence of AF. In the absence of elevated complement components, no statistically confirmed association was found between a high CRP level and AF.

Adult↗
PubMed1992

Complement C1qB and C4 mRNAs responses to lesioning in rat brain.

These data show the presence of mRNAs for two complement components (C) in the adult rat brain and describe their responses to experimental lesions. Cortical deafferentation caused elevations in striatal C1qB and C4 mRNAs that coincided temporally and overlapped anatomically with the course of degeneration of corticostriatal afferent fibers. By in situ hybridization, C1qB mRNA in the lesioned striatum was colocalized to cells immunoreactive for CR3, a complement receptor found on microglia-macrophages. The mRNA for SGP-2, a putative C inhibitor in rat, showed parallel changes. Similarly, in hippocampus and other brain regions, kainic acid lesions increased C1qB mRNA. The data suggest that microglia-macrophages and possibly other cells in rat brain rapidly up-regulate C-mRNAs in response to deafferentation and local neuron injury. These experimental responses provide models to analyze changes in C components during Alzheimer's disease and other chronic neurodegenerative conditions.

Animals↗
PubMed1999

Rapid onset monoclonal gammopathy in cutaneous lupus erythematosus: interference with complement C3 and C4 measurement.

Accurate nephelometric immunoassay requires both the analyte and the calibration standard to have the same molecular mass. Alteration in the size of the analyte can affect light scatter and yield erroneous results. We report a case where an autoantibody, a monoclonal IgM with immunoconglutinin activity, interfered with the nephelometric quantitation of plasma complement components C3 and C4.

Adult↗
PubMed1982

Complement proteins C2, C4 and factor B. Effect of glycosylation on their secretion and catabolism.

Tunicamycin, an inhibitor of N-acetylglucosaminylpyrophosphopolyisoprenol-dependent glycosylation, was used to study the effect of glycosylation on the synthesis, post-translational modification, secretion and function of the complement proteins that are associated with the major histocompatibility complex in humans, mice and guinea pigs. Tunicamycin blocked glycosylation of pro-C4, C2 and factor B and inhibited secretion of the corresponding native complement proteins synthesized by guinea-pig peritoneal macrophages in tissue culture. In addition, underglycosylated pro-C4 was more rapidly catabolized intracellularly than the corresponding fully glycosylated pro-complement protein. C4 protein secreted by cells incubated with tunicamycin had approximately the same specific biological activity as the protein obtained from control culture media, suggesting that carbohydrate is not required for its activity in immune haemolysis. Direct studies of carbohydrate incorporation and the tunicamycin effect suggested an unequal distribution of sugar among the C4 subunits, with maximal incorporation of carbohydrate into alpha-, and less into the beta-chain of the native protein.

Animals↗
PubMed2003

Complement activation by direct C4 binding to thyroperoxidase in Hashimoto's thyroiditis.

Biosynthesis of thyroid hormones is an oxidative process that generates reactive oxygen species (ROS) and involves thyroperoxidase (TPO) that is one of the main autoantigens involved in autoimmune thyroid diseases. The ectodomain of TPO consists of a large N-terminal myeloperoxidase-like module followed by a complement control protein (CCP)-like module and an epidermal growth factor-like module. The presence of these two additional gene modules suggests that they may play some crucial, hitherto unsuspected role associated with thyroid function. Because the CCP module is a constituent of the molecules involved in the activation of C4 complement component, we investigated the possibility that C4 may bind to TPO and activate the complement pathway in autoimmune conditions. We showed that TPO via its CCP module directly activated complement without any mediation by Ig. We suggested that this additional complement pathway requires the production of ROS and specially hydroxyl radicals that aggregate TPO and oxidize methionines of C4. Moreover, we found, in patients with Hashimoto's thyroiditis, that thyrocytes overexpress C4 and all the downstream components of the complement pathway. These results indicate that TPO has some as yet unknown function, which may contribute along with other mechanisms to the massive cell destruction observed in Hashimoto's thyroiditis. Investigating this complement pathway, therefore, would provide an excellent means of reaching a better understanding of the etiology of other degenerative diseases.

Acute Disease↗
PubMed1991

Genetic polymorphism of the C4 component of human complement in the Slovak population.

The distribution of C4 phenotypes and gene frequencies were studied in 104 genetically unrelated persons of Slovakia using high-voltage agarose gel electrophoresis with subsequent immunofixation. Five C4A alleles and three C4B alleles were detected. The gene frequencies were as follows: A2 = 0.0576, A3 = 0.7644, A4 = 0.0336, A6 = 0.0625, AQ0 = 0.817, B1 = 0.7836, B2 = 0.1009, BQ0 = 0.1153. The C4AQ0 and C4BQ0 alleles established by densitometry appeared in the Slovak population in 16.34% and 23.07%, respectively.

Adolescent↗
PubMed1980

Serum concentrations of C3 and C4 of the complement system in patients with chronic obstructive pulmonary disease.

In a search for host factors for the complex multifactoral disease, chronic obstructive pulmonary disease, we compared some major components of the complement system in 111 subjects with forced expiratory volumes in 1 sec less than 70% of predicted (index subjects) to those in 111 subjects matched as pairs for age, sex, smoking, and occupation having forced expiratory volumes in 1 sec more than 85% of predicted normal. Significantly lower blood levels of C3 and C4 were found in the index subjects (p less than 0.001). Among the index subjects there was a significant correlation between chronic cough and expectoration and low C3 and C4. There was not a significant correlation between low values and the frequency and severity of past respiratory infections. Levels of serum B globulin fraction, in which C3 and C4 migrate, were not different between the index and control subjects.

Complement C3↗
PubMed1998

New Australian aboriginal complotypes characterised by increased C4 gene copy number.

Complement component C4 genes are located within the central region of the human MHC. The genomic arrangement of these genes is complex, with each chromosome usually encoding either one or two C4 genes. C4 allotyping of a group of Western Australian Aborigines demonstrated certain discrepancies in the densitometric ratios between the C4A4 and the C4A3 protein bands; however, the mechanism causing the increase in density of the C4A4 band was unknown. Our aim was to determine whether the increase in densitometry was due to an increase in the expression of the C4A4 isotype, or whether these individuals carried a new complotype characterised by an increased gene copy number. Using pulsed-field gel electrophoresis and Taq I RFLP analysis we will show that the apparent increase in C4A4 protein expression was due to the existence of new, previously uncharacterised Aboriginal complotypes defined by at least three C4 genes. Segregation analysis from an extensive family suggests that one of the new C4 complotypes is likely to contain the duplicated C4A4 isotype together with a C4B2 gene (C4A4, C4A4, C4B2) and is the first such chromosomal arrangement seen in this population group.

Australia↗