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At least 199 records · Page 11Linked to original sources
PubMed1981

Family studies of complement C4 and HLA in man.

At least 12 different C4 gene products with a three band pattern have been identified after electrophoresis of sera pretreated with neuraminidase. Segregation analysis showed at least 12 different C4 haplotypes (or supergenes), of which five represent a single gene product and seven are duplications each composed of an F and an S gene. The data analyzed with respect to linkage showed one recombinant between the C4 and HLAB loci in 154 meioses giving a map distance of C4 HLAB of 0.6 cM. Another recombinant between the C4 and the HLAD loci was found in 101 meioses giving a map distance of C4 HLAD of 1.0 cM. Linkage disequilibrium was found between at least eight C4 haplotypes and certain alleles at the HLAB as well as the HLAD loci. Examinations of 15 families selected through a proband with HLAA 25, HLAB 18 and C2Q0 showed that in almost all cases a slight variant of the C4 supergene F3S2 followed the haplotype HLAA25 HLAB18 C2Q0. No associations were found between the two duplications of C4F3 C4S2 and C4F3 C4S1 and the loci. These findings may indicate that these C4 haplotypes were the original ones preceding the other C4 haplotypes.

Adult↗
PubMed1981

HLA genotypes and HLA-linked genetic markers in Italian patients with classical 21-hydroxylase deficiency.

HLA genotype and HLA-linked marker data for 40 unrelated patients from central Italy and 2 unrelated patients from Sardinia with congenital adrenal hyperplasia due to 21-hydroxylase deficiency (21-OH-def) were analyzed. The results confirm that the HLA-linked 21-OH-def gene is associated with several different HLA determinants and complete HLA haplotypes, although the only determinant with significantly increased frequency was the complement C2 allele C2B. The HLA antigens B8 and DR3 were found in significantly decreased frequencies. The haplotype A3, Cw6, Bw47, BfF, DR7, which is exceptionally rare in the general population but which has been found in many other 21-OH-def patients from diverse geographical origins, was also found in one of the Italian patients. This and other HLA haplotype associations found among the Italian patients may represent mutations that have occurred on HLA haplotypes with genetic linkage disequilibrium or, alternatively, may represent mutations that have not yet had time to become randomly associated with different HLA complex determinants. The marked negative associations with B8 and DR3 could, however, result from an interaction between the gene products of the HLA complex and the 21-OH-def phenotype.

Adrenal Hyperplasia, Congenital↗
PubMed1986

Significance of the Ro antigen system.

Knowledge about antibodies to the Ro/SSA and La/SSB antigens has expanded greatly. Recognition of these antibodies was probably achieved 25 years ago but their macromolecular structure, clinical associations, and genetic relationships have come to light only in the past 7 years. It seems clear that these antibodies have a special place in the nosology of SLE and SS and that in certain instances (e.g., neonatal LE) the antibodies play a direct pathogenic role, while in other circumstances (e.g., vasculitis, nephritis, SS) tissue damage might result from immune complex deposition on vascular structures. Certainly, the latter problems will be active areas of investigation in the coming years. If the pace of recent progress continues, many of the questions raised in this review should soon have clear answers.

Antibodies, Antinuclear↗
PubMed1990

A BF subtype "Fb1" is a marker gene of some Mongoloid populations.

A factor B subtype, BF*Fb1, was first detected in Japanese by using isoelectric focusing or agarose gel electrophoresis in Tris/glycine/Veronal buffer. Our previous studies suggested that BF*Fb1 may be characteristic of some of Mongoloid populations. To investigate further distribution of BF*Fb1, samples randomly collected from Japanese in Yonaguni island of Japan and Cambodian were tested. BF*Fb1 was not observed in a Cambodian population whereas in a Japanese population of Yonaguni island, BF*Fb1 occurred at a frequency five times as high as those in main islands of Japan. In paternity cases, a Korean family with three offsprings was shown to transmit BF*Fb1 from the accused man to one of the offsprings. These data strongly indicate that BF*Fb1 is a marker gene for some of Mongoloid populations.

Alleles↗
PubMed1985

Granulocyte adhesion to nephritic glomeruli through recognition of activated C4 and C3 in immune deposits.

Sections of rat kidney with bovine serum albumin nephritis were incubated either with a single component of complement or with several components in sequence and then reacted with granulocytes. The average number of granulocytes bound to a nephritic glomerulus was elevated in sections incubated with C4 or C3 and increases were most significant when C14, C142 or C1423 were incubated.

Animals↗
PubMed1983

Synthesis of complement by macrophages and modulation of their functions through complement activation.

During the last decade considerable progress has been made to characterize intimate functional links between macrophages, a major cellular component of immunoinflammatory responses, and the complement system representing the major humoral mediator of inflammation. Macrophages of various species and tissue sites have been shown to synthesize and release most of the complement components providing these cells with their own "pericellular" complement system. Circumstantial evidence for the assembly of both classical and alternative pathway convertases has been adduced. An intricate network of feedback loops involving endogenous and extrinsic factors operates to adjust complement production to acute requirements, for example augmenting production in the face of accelerated turnover at sites of inflammation, and returning it to baseline levels once the inflammatory stimulus has subsided, in order to maintain a fine-tuned balance. The molecular mechanisms underlying regulation of complement synthesis by macrophages are beginning to be elucidated by use of gene technology. On the other hand, complement activation products exert a number of effects on macrophages via specific surface receptors causing internalization of offending agents, microbes, and immune complexes, promotion of intracellular killing, controlling migration behavior, inducing release of potent biologic substances such as lysosomal enzymes, arachidonic acid metabolites, and interleukin 1. In these interactions, two important humoral mediator systems of inflammation, the complement system and the arachidonic acid cascade, are functionally linked at the level of the macrophage. Stimulation of the release of immunomodulating compounds from macrophages invoke a role for complement in immune regulation. This multifaceted interplay is of particular importance considering the mobility of macrophages that allows them to gain almost unrestricted access to sites of ongoing immunoinflammatory responses. The time seems to have come to abandon the petrified thinking in socalled systems as, for instance, humoral versus cellular, specific versus unspecific, and to proceed to interlocking functions guided by physiology proper.

Anaphylatoxins↗
PubMed1978

A case of Menetrier's disease associated with protein-losing gastropathy and abnormal serum complement profile.

A 44-year-old man with Menetrier's disease associated with protein-losing gastropathy and with abnormal serum complement profile is reported. He was treated by an antifibrinolytic compound tranexamic acid (trans-AMCHA) since he was found to have elevated fibrinolytic activity in the biopsied gastric mucosa. The therapy brought his serum protein from 3.8 g/dl to 5.6g/dl, however could not reduce his mucosal disorder. Substitution of a placebo for trans-AMCHA resulted in marked depression of his serum protein to 3.7 g/dl. It was concluded that trans-AMCHA was effective in raising his serum protein to a certain extent but failed to block the vicious circle of "mucosal disorder", "increased tissue fibrinolysis" and "hypoproteinemia" (Kondo, M. et al. Gastroenterology 70, 1045, 1976). Abnormal serum complement profile seen in this patient was found to be due to cold activation of the classical complement pathway (Kondo, M. et al. J. Immunol. 117, 486, 1976). Although no correlation between the phenomenon and Menetrier's disease has been clarified yet, the appearance of wheezing as in asthma when exposed to cold suggested that cold activation of complement occurred in vivo and resulted in increasing of the vascular permeability in the lungs.

Adult↗
PubMed1988

Major histocompatibility complex associations with systemic lupus erythematosus.

This study focused on clinical subsets within systemic lupus erythematosus (SLE) in order to identify more homogeneous patient groups in which to define disease susceptibility gene(s). Analysis of the major histocompatibility complex gene products and genes with major histocompatibility complex class II and class III locus-specific probes and oligonucleotide probes for selected human leukocyte antigen DQ-beta alleles showed significant increases of human leukocyte antigen DR2 and the rare DQ-beta allele DR2-DQw1.AZH in the lupus nephritis patients compared with lupus patients without renal disease (relative risk = 8.3). C4A null was detected in one third of all of the SLE patients. In two thirds of the C4A null patients this was due to a DR3-associated C4A gene deletion. The remaining third may have a regulatory defect and this was DR2-associated. DR4 was significantly decreased in the nephritis patients in comparison with the non-renal SLE patients (relative risk = 0.3). A novel DQ-beta gene has been sequenced from two SLE patients that has not been observed in the normal population. Potential implications of these findings are discussed.

Complement C2↗
PubMed1984

Arachidonic acid-mediated and serum-opsonized-zymosan-mediated inhibition of complement production by macrophages. Lack of requirement for endogenous arachidonic acid metabolites.

The ability of exogenous prostaglandins to inhibit complement production (CP) by monocytes and macrophages (M phi) suggests that endogenous arachidonic acid metabolites produced by these cells may also regulate their rate of CP. We assessed the regulatory influence of endogenous metabolites on CP by M phi utilizing exogenous arachidonic acid and serum-opsonized zymosan as stimulators of production of cyclooxygenase and lipoxygenase metabolites. The results of this study show that (i) the inhibition of CP caused by both agents is is independent of arachidonic acid metabolites, suggesting that endogenously produced metabolites do not influence CP, and (ii) arachidonic acid and serum-opsonized zymosan inhibit production by independent mechanisms.

Animals↗