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R Mierau

Publications and source records attributed to R Mierau.

31 records · Page 2Linked to original sources
PubMed1987

HLA-DR4 and Gm 1;21 haplotypes are associated with pseudolupus induced by venopyronum dragées.

The phenotypic frequencies of human major histocompatibility complex class I, II, and III antigens and immunoglobulin allotypes (Gm factors) were determined in 56 patients (55 women, 1 man) who had lupus-like disease induced by venopyronum dragées. The findings in these patients were compared with those of a control group. We found a significant increase of HLA-DR4 (57.1% versus 26.5%, relative risk [RR] 3.7) and a decrease of HLA-DR3 (3.6% versus 19.1%, RR 0.16) in the patient group. In addition, the haplotype Gm 1;21 (60.7% versus 32.9%, RR 3.2), and the phenotype Gm 1,3;5,21 (46.4% versus 25.8%, RR 2.5) were significantly increased. Both the haplotype Gm 1;21 and the phenotype Gm 1,3;5,21 are associated with HLA-DR4 in pseudolupus patients but not in controls. The coincidence of HLA-DR4 and Gm 1;21 markedly increases the risk of acquiring pseudolupus (RR 6.9). We conclude that the pathogenesis of pseudolupus is influenced by at least 2 independent genetic factors. A similar HLA association has been described in hydralazine-induced lupus, and this suggests a common pathogenic mechanism.

Adult↗
PubMed1987

Antigenic determinants shared between HLA-A, -B, -C antigens and H-2 class I molecules modified by bovine beta-2 microglobulin.

The specificity of the mouse class I-specific antibody COB6-3 was examined in detail. It was found to react with the mouse class I molecules H-2Db, Kd, and Qa-2, and with human HLA-A, -B, -C antigens. The specificity pattern of COB6-3, despite its different origin, was similar to that of the monomorphic HLA class I-specific antibody W6/32. Cross-inhibition studies show that on human cells the antigenic determinants recognized by the two antibodies are situated close together and may be identical. On mouse cells, reactivity of both antibodies was generated upon replacement of mouse beta-2 microglobulin (B2m) with its bovine counterpart, but differences in specificity were observed using human B2m.

Animals↗
PubMed1987

HLA-DR4 and Gm(1,3;5,21) are associated with U1-nRNP antibody positive connective tissue disease.

Patients with U1-nRNP antibodies (n = 35, 31 female, four male) were typed for HLA-A, -B, -C, and -DR antigens and IgG heavy chain allotypes G1m(1), -(2), -(3), G3m(5), and -(21). The patient group was clinically heterogeneous. Four met the American Rheumatism Association criteria for systemic lupus erythematosus, six for progressive scleroderma, and 14 for rheumatoid arthritis. Sicca syndrome was present in seven cases. Twenty three had overlapping features compatible with mixed connective tissue disease (MCTD). Healthy blood donors served as controls for HLA typing (n = 64), Gm typing (n = 228), or both (n = 56). Sixty six per cent of the patients with U1-nRNP antibodies were DR4 positive compared with 28% of the controls (relative risk = 4.9, p = 0.00053). The Gm(1,3;5,21) phenotype was found in 46% of the patients and 25% of the controls (relative risk = 2.47, p = 0.0247). Within the patient group Gm(1,3;5,21) was found only in DR4 positive individuals. The coincidence of HLA-DR4 and Gm(1,3;5,21) increases the relative risk values to 8.0 (compared with the group with neither risk factor). DR4 and Gm(1,3;5,21) primarily seem to be related to U1-nRNP antibody formation and not to disease expression. Patients with or without MCTD did not differ with respect to DR4 or Gm(1,3;5,21) frequency. Disease onset was earlier in patients with HLA-DR4/Gm(1,3;5,21) than in patients without both markers (mean 27.9 v 40.1 years; p less than 0.05).

Adolescent↗
PubMed1986

Increased frequency of Gm(1,2;21) phenotype in HLA-DR4 positive seropositive rheumatoid arthritis.

Ninety-four patients with seropositive rheumatoid arthritis (RA) were typed for HLA-A, B, C and DR antigens and for immunoglobulin G (Gm) allotypes. Isolated IgG from patient serum was used to avoid interference of IgM rheumatoid factor (RF) with Gm typing in sera with high IgM-RF titer. Besides the association of seropositive RA with the antigen DR4 and an earlier disease onset in DR3/DR4 heterozygotes, we found the uncommon Gm phenotype Gm(1,2;21) significantly more often in our patient group than in healthy controls. Combination of HLA-DR and Gm data shows that individuals with both DR4 and Gm(1,2;21) are at a particularly high disease risk.

Adult↗
PubMed1985

Interference of IgM rheumatoid factor with nephelometric C-reactive protein determinations.

Different nephelometric assay systems for quantitation of C-reactive protein (CRP) were compared with radial immunodiffusion (RID) and tested for their susceptibility to interference by serum IgM rheumatoid factor (RF). In 3 nephelometric assays, RF was found to elevate CRP values. Sera with high RF content from patients with rheumatoid arthritis gave significantly higher CRP values by nephelometric assay than by RID; the addition of purified RF to RF-negative sera increased CRP values markedly; and removal of RF from sera corrected falsely elevated CRP values. This interference by RF is explained by the action of human RF as a (secondary) antibody reacting with complexed mammalian IgG anti-human CRP in the assay. In this way the nephelometric signal is enhanced to give falsely elevated CRP values. In contrast, the gel diffusion RID method does not suffer from this non-specific interference.

Arthritis, Rheumatoid↗
PubMed1980

Antigen-specific receptor molecules isolated from murine T lymphocytes.

Hapten-specific receptor material can be isolated from sensitized murine T and B lymphocytes by the use of hapten-coupled nylon discs. The structural element shared between T and B cell receptors is the variable region of immunoglobulin heavy chains (VH), while known constant immunoglobulin domains appear not to be part of the T cell receptor molecule. The rules governing VH expression (i.e. NPb-idiotype expression) in the B and the T cell compartments are, however, different. Allotype-linked VH (idiotype) expression on T cell molecules was used in genetic reconstitution experiments to prove that the material under study is an endogenous T cell product. With the data available it seems reasonable to view the T cell molecules as representing surface receptors for antigen although this point needs further investigation.

Animals↗
PubMedDate not supplied

[Diagnostic significance of scleroderma and myositis-associated autoantibodies].

In more than 95% of patients with systemic sclerosis and in about 60% of patients suffering from idiopathic inflammatory myopathies autoantibodies directed at different nuclear or cytoplasmic antigens can be detected with different methods. Scleroderma-associated autoantibodies can be visualized as antinuclear antibodies (ANA) by immunofluorescence assays using cultured monolayer cells. In case of a negative ANA result the diagnosis of systemic sclerosis is unlikely. In individual patients the different autoantibodies (against DNA topoisomerase I (Scl-70), centromeric antigens, fibrillarin, To (Th), RNA polymerases, NOR-90, U1-nRNP, PM-Scl, Ku) are mutually exclusive. They can be detected early in the course of diseases, most often are persistent, and are closely associated with immunogenetic markers. They are characteristic for distinct subsets of patients homogeneous in clinical manifestations as well as in disease outcome. Myositis-associated autoantibodies are directed to nuclear (about 60% of myositis patients; PM-Scl, Mi-2) or cytoplasmic antigens (about 35-40%; Jo-1 and other aminoacyl-tRNA-synthetases, signal recognition particle (SRP), KJ and others) and likewise are related to distinct clinical, prognostic, and immunogenetic traits leading to the description of characteristic antibody-based syndromes. Based on published results and on our own investigations, the diagnostic potential of scleroderma- and myositis-associated antibodies is evaluated and a new classification of systematic myositic and sclerodermatous disease is proposed.

Antibodies, Antinuclear↗