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PubMed1991

Heat shock protein 70 (HSP70) and complement C4 genotypes in patients with hyperthyroid Graves' disease.

The genetic polymorphisms of the heat shock protein 70 (HSP70) and complement component C4 were investigated in 90 patients with hyperthyroid Graves' disease and 92 normal control subjects. The 8.5-kb PstI HSP70 allele was strongly associated with Graves' disease when compared with controls (P less than 0.001). The presence of the 8.5-kb PstI HSP70 allele was strongly associated with a deletion of the C4A gene in both patients and controls (P less than 0.0003 and P less than 0.00005 respectively). However, in the absence of C4A gene deletion, the frequency of the 8.5-kb PstI HSP70 allele was still significantly higher in patients when compared with controls (P less than 0.04). These results suggest that the HSP70 locus may have an immunological role to play in autoimmune hyperthyroid Graves' disease.

Alleles↗
PubMed1991

[Problems in the determination of immunocomplexes. VI. Changes in the levels of C4 complement and IgG in the precipitation of immunocomplexes using polyethylene glycol].

The authors modified the method for the assessment of circulating immunocomplexes by assessing changes in the concentration of IgG and C4 components of complement in the precipitate after adding polyethylene glycol. The method was tested on a series of samples, the scatter of values for the healthy population was assessed and the results were compared with the PEG method elaborated in the Institute for Clinical and Experimental Medicine.

Antigen-Antibody Complex↗
PubMed1992

Molecular heterogeneity of the fourth component of complement (C4) and its genes in vitiligo.

In view of evidence suggesting vitiligo is an autoimmune disease, we investigated whether vitiligo is associated with inherited deficiencies of the fourth (C4) and second (C2) component of complement and with certain human leukocyte antigens (HLA). Analysis of functional activities of C4 and C2 in sera of patients with vitiligo (n = 42) showed that 17% of them had a heterozygous C4 deficiency and 5% had a heterozygous C2 deficiency. In the normal control group (n = 30), 3% had a heterozygous C4 deficiency and none had a C2 deficiency. C4 typing by Western blot analysis showed the frequency of the C4A*Q0 allele in the vitiligo patient group to be close to normal. However, the frequency of one C4B*Q0 allele was three times higher, and that of two C4B*Q0 alleles five times higher in the vitiligo patient group than the reported frequencies in normal control groups. Southern blot analysis of Taq1 digests of DNA using C4 and 21-hydroxylase probes showed that two patients with two C4B*Q0 alleles had a deletion of a 21-OHA-C4B segment. In the other patients, having one or two C4B*Q0 alleles, these null alleles probably occurred due to a loss of C4 gene expression. HLA analysis did not show any allelic association of C4A*Q0 or C4B*Q0 with any HLA antigen in vitiligo, but confirmed the previous findings of a negative association with HLA-DR3 and a positive association with HLA-DR4. These results suggest that abnormalities of the C4B gene and the above-mentioned associations with HLA antigens may be some of the risk factors in vitiligo.

Adrenal Hyperplasia, Congenital↗
PubMed1990

Importance of the alpha 3-fragment of complement C4 for the binding with C4b-binding protein.

The human regulatory complement component C4b-binding protein (C4BP) is a multimeric plasma protein, which regulates the classical pathway of the complement system. C4BP functions as a cofactor to factor 1 in the degradation of C4b and accelerates the decay rate of the C4b2a complex. Previously, we have demonstrated that monoclonal antibodies (C4-2 and 9) directed against the alpha'-chain of C4b inhibit the binding of C4b to C4BP. In order to identify the structural domain of C4b that binds C4BP, proteolytic fragments of C4 were generated with trypsin and Staphylococcus aureus V8 protease. Sodium dodecyl sulfate polyacrylamide gel electrophoresis, immunoblotting and amino acid sequence analysis of the proteolytic fragments reactive with the anti-C4 mAb's revealed that the residues Ala738-Arg826 of the alpha 3-fragment of C4b are important for the interaction with C4BP.

Amino Acid Sequence↗
PubMedDate not supplied

A rare TaqI polymorphism in a human complement C4 gene is caused by an additional restriction site in the first intron.

We studied the configuration of the complement C4/CYP21 (steroid 21-hydroxylase) region of the human major histocompatibility complex in patients suffering from congenital adrenal hyperplasia (CAH) and in the general population in The Netherlands, using C4 and CYP21 probes and the restriction enzymes TaqI and Bg/II. We found a rare TaqI 3.9-kb restriction fragment in the mother of a CAH patient, and present evidence that this polymorphism is caused by an additional restriction site in the first intron of a complement C4 gene.

Adrenal Hyperplasia, Congenital↗
PubMed1978

[Study of C3 and C4 complement components of synovial fluids in connective tissue diseases (author's transl)].

C3 and C4 levels and the relative concentration of C3 degradation products were measured in fifty pairs of synovial fluids and sera of patients who suffered from different connective tissue diseases. Inverse correlation between C4 level and C3 breakdown products were found in synovial fluids of different groups. Compared to the other groups of patients, the highest increase of C3 degradation was found in RA. patients and it occurred in the SF all of these patients. In arthrosis cases we failed to find any degradation of C3. Of the seven investigated ankylosing spondylitis only two showed some degree of activation of C3 in the SF. Our results suggest that the occurrence and degree of degradation of C3 complement component is a valuable laboratory parameter in the study of connective tissue diseases.

Arthritis↗
PubMed1990

Restriction fragment length polymorphism of complement C4 in Japanese patients with rheumatoid arthritis and normal Japanese.

Restriction fragment length polymorphism (RFLP) of the two genes for complement C4A and C4B was studied in 56 Japanese patients with rheumatoid arthritis (RA) and 161 normal individuals. HindIII digestion revealed six common patterns, from which the segregation of three common RFLP-types were deduced; 32-15 kb, 32-25 kb, and 32-20-13-6.5 kb. The last type showed positive associations with C4B5 and HLA-DR4. In the RA patients, an increase of this type was found as well as a decrease of the 32-15 kb/32-25-15 kb heterozygotes.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Antigenic determinants of C3 and C4 complement components on washed erythrocytes from normal persons.

Well-washed erythrocytes from normal persons were agglutinated by antisera to C3, C3d, and C4, and this agglutination was specifically inhibited by the corresponding C3 or C4 protein. C3 and C4 antigenic determinants were present on the red blood cells of freshly shed blood promptly anticoagulated with EDTA, heparin, ACD, or CPD, and no significant changes in degree of agglutination were observed on storage of EDTA or CPD blood for two weeks at 4 C. Marked differences in degree of agglutination by anti-C3, anti-C3d, and anti-C4 were observed when erythrocytes of 16 normal persons were assayed, and significant correlations were obtained when the quantitative results with any two antisera were compared. Anti-C3c did not agglutinate erythrocytes from normal persons, suggesting that the C3 antigens detected on normal cells are carried by the C3d fragment. To avoid significant agglutination of the erythrocytes from some normal persons, very dilute preparations of anti-C3, -C3d, and -C4 had to be used for instrumented diagnostic direct antiglobulin tests. Stronger reagents could be used for indirect antiglobulin tests when the result of a suitable control could be subtracted.

Animals↗
PubMed1992

Prolonged clinically asymptomatic evolution after HIV-1 infection is marked by the absence of complement C4 null alleles at the MHC.

The length of time after which persons infected with HIV-1 progress to AIDS is variable. Certain alleles at the MHC have been shown to influence negatively the clinical outcome of HIV-1-infected persons and to be associated with special clinical manifestations. We investigated the MHC class I, class II and class III antigens in 54 Caucasian HIV-1-infected persons. The MHC profile of individuals with a prolonged period before AIDS is marked by a lower frequency of C4 null alleles.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Genetic studies of complement C4 in man.

A C4 variant found in about 5% of the population is described. The fast-moving part of this variant is governed by an allele (Fx) codominant to F. The Fx allele is in very strong linkage disequilibrium with HLA-B17 as the linkage disequilibrium parameter accounted for nearly 100% of the haplotype frequency of B17,Fx. The strong association is also evidenced by the study of 11 families segregating for the Fx allele. There was no instance of recombination between C4 and HLA in 36 informative meioses.

Adult↗
PubMed1992

Analysis of complement C4 loci in Caucasoids and Japanese with idiopathic membranous nephropathy.

Deletion of the HLA class III complement gene, C4A, has been linked with susceptibility to a number of autoimmune diseases. In this study, we show a strong positive association between C4A gene deletion and development of idiopathic membranous nephropathy (IMN) in European Caucasoids [patients, 17/27 (63%); healthy controls, 13/65 (20%); RR 6.8; P = 0.003]. To clarify whether C4A deletion is an independent risk factor for IMN or is increased secondarily to the Caucasoid HLA A1, B8, DR3 extended haplotype, we examined the frequency of C4A deletion in Japanese patients, in whom the disease is associated with another HLA haplotype (DR2-DQw1). Analysis of 31 Japanese patients and 46 healthy controls showed that C4A deletion was present in only one patient (3%) and one control (2%). In addition, examination of the C4B locus in Japanese patients showed that there was no significant increase in the estimated frequency of C4B deletion in patients against controls (31 vs. 27%) and no difference in the frequency of the C4B long gene (73 vs. 87%) or C4B short gene (77 vs. 78%). We conclude that although C4A deletion confers significant risk of IMN in Caucasoids, there is no significant association between C4 polymorphism, as detected here, and risk of IMN in Japanese. This suggests that either C4A deletion is irrelevant to the pathogenesis of IMN or that more than one genetic mechanism is involved.

Asian People↗
PubMed1992

Lack of deletion of complement C4 and steroid 21-hydroxylase genes in Japanese patients with primary Sjögren's syndrome.

A null allele at C4A (C4AQO) is associated with primary Sjögren's syndrome (SS) in Japanese. Since a deletion of the C4A and CyP21A genes is reported to account for C4AQO in patients with systemic lupus erythematosus (SLE) in Caucasians, we studied the restriction fragment length polymorphism (RFLP) of genomic DNA to determine whether similar deletions of the C4A and CyP21A genes occur in Japanese patients with SS. Patients with C4AQO did not show the extensive deletion of C4A and CyP21A, which would be recognized by the appearance of 8.5 kb/HindIII and 6.4 kb/TaqI fragments hybridizing with a C4 probe. It is yet to be shown whether the lack of expression of C4A genes in Japanese patients with primary SS is due to point mutations, or to small deletions or insertions that were not detected by the RFLP approach.

Alleles↗
PubMed1992

Complement C4 null alleles as a marker of gold or D-penicillamine toxicity in the treatment of rheumatoid arthritis.

C4 null alleles and HLA-DR antigens were defined in 48 rheumatoid arthritis (RA) subjects who had developed renal or heamatological side effects to gold or penicillamine, as compared to 33 RA subjects who had received the drugs for similar time periods without developing side effects. A C4A null allele was found in 56% of subjects with and 31% of those without side effects (P = 0.027, relative risk 2.8). A similar but statistically non-significant trend was observed with the C4B null allele (P = 0.64) resulting in a higher risk of drug toxicity in rheumatoid patients bearing either a C4A or C4B null allele (relative risk 5.7). Frequencies of DR3 and DR4 were similar in the two groups.

Alleles↗