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Biomedical subjects

J M Rasmussen

Publications and source records attributed to J M Rasmussen.

At least 37 records · Page 2Linked to original sources
PubMed1989

The influence of C3-coated homologous erythrocytes on pokeweed-mitogen-induced polyclonal differentiation of human B cells.

The present study was undertaken in order to test the hypothesis that homologous erythrocytes (E) coated in vivo with C3d could modulate the immunoglobulin (Ig) synthesis of human peripheral blood mononuclear cells (PBMC), stimulated with pokeweed mitogen (PWM) in vitro. E from healthy individuals were found to enhance markedly the Ig synthesis of PMBC cultures stimulated with suboptimal doses (0.01 microgram/ml) of PWM. E coated in vivo with increasing amounts of C3d (1.4-6.3 times the amounts on normal E), obtained from patients with systemic lupus erythematosus, failed to induce any significant increase in Ig synthesis of PBMC cultures stimulated with suboptimal PWM doses, compared with cultures co-stimulated in parallel with normal E. In contrast, an increase in IgM and IgG synthesis was observed in about 50% of PBMC cultures from different donors when stimulated with PWM in the presence of E coated with C3b in vivo (from a patient with congenital factor I deficiency), compared with the Ig synthesis in cultures co-stimulated in parallel with normal E. In contrast to the inability of C3d-coated E to modulate B-cell proliferation, the monoclonal anti-CR2 antibody OKB7 was found to be mitogenic for unstimulated peripheral B cells.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1989

Enhanced binding of immune complexes processed by erythrocyte CR1 (CD 35) receptors to purified CR2 (CD 21) receptors from tonsillar mononuclear cells.

The binding of immune complexes (IC) opsonized by serum complement (C) and IC processed by CR1 (CD 35) receptors on human erythrocytes (E) to purified CR2 (CD 21) receptors was compared. Soluble CR2 was prepared from tonsillar mononuclear cells and purified by antibody affinity chromatography. Solid phase CR2 as well as CR2 subjected to PAGE and blotted onto nitro-cellulose membranes bound 125I-labelled BSA anti-BSA IC which had been opsonized by C and processed by CR1 up to ten times more efficiently than IC reacted with serum only. Radiolabelled monomeric C3d also bound to solid phase CR2. The binding of IC to purified and solid phase bound CR2 could be inhibited by anti-CR2 antibodies or by preincubation of the IC with polyclonal antibodies reacting with C3d or C3b/iC3b. Thus, both C3dg and iC3b appeared to mediate binding of IC to CR2. Preincubation of solid phase CR2 with purified monomeric C3d did not inhibit the subsequent binding of E-CR1 processed IC. The data indicate that E-CR1 have an important role in generating IC which bind effectively to CR2 receptors on B lymphocytes.

Animals↗
PubMed1988

Inefficient binding of IgM immune complexes to erythrocyte C3b-C4b receptors (CR1) and weak incorporation of C3b-iC3b into the complexes.

The binding of soluble complement-reacted IgM immune complexes (IC) to erythrocyte (E) C3b-C4b receptors (CR1) and the incorporation of C3b-iC3b into solid phase IgM-IC was investigated. The optimal binding of liquid phase IgM-IC to E-CR1 was obtained with IC formed at moderate antibody excess, but the binding was low (2-3%) when compared to the binding of the corresponding IgG-IC (50-60%). Solid phase IC were prepared by coating microwells with heat-aggregated bovine serum albumin (BSA) followed by incubation with rabbit IgM anti-BSA antibody. The IC were reacted with human serum at 37 degrees C. The binding of C3b-iC3b was determined by use of biotinylated F(ab')2 antibodies to C3b-C3c and avidin-coupled alkaline phosphatase. The incorporation of C3b-iC3b into solid-phase IgM-IC increased when increasing amounts of IgM antibody were reacted with the antigen. The binding reaction was slow, reaching a maximum after about 2 h at 37 degrees C. The binding of C3b-iC3b to the IgM-IC was remarkably inefficient when compared to the incorporation into IgG-IC reacted with the same amounts of BSA-precipitating antibody.

Animals↗
PubMed1988

Quantification of C3dg/Epstein-Barr virus receptors on human B cells and B cell lines.

The expression of C3dg/Epstein-Barr virus receptors (CR2) on human peripheral blood and tonsillar B lymphocytes and Raji cells was quantified by measuring binding of unlabeled monoclonal anti-CR2 antibody (OKB7 and HB-5) in an indirect immunoenzymatic assay. Scatchard analysis of saturation binding curves revealed that Raji cells on the average express about 22,000 and 17,000 binding sites, with mean affinity constants of 9.9 X 10(10) and 8.7 X 10(10) M-1 for OKB7 and HB-5, respectively. Tonsillar mononuclear cells (TMC) expressed 16,700 and 17,600 binding sites for OKB7 and HB-5, respectively, with a significantly lower affinity constant for HB-5 (3.2 X 10(10) M-1) than for OKB7 (9.0 X 10(10) M-1). On the average 34% of E- peripheral blood mononuclear cells (PBMC) from healthy donors and 49% of TMC expressed the CR2 antigen. When correcting for the fraction of CR2-positive cells, the mean CR2 density was 12,600 on E- PBMC (n = 10) and 34,000 on TMC (n = 4).

Animals↗
PubMed1988

An epidemic outbreak of group B meningococcal disease on the Faroe Islands.

An epidemic of group B meningococcal disease on the Faroe Islands is described. A peak annual incidence of 95 cases/100,000 was reached in 1981. The time at which the epidemic commenced cannot be determined due to inadequate diagnostic facilities, but was presumably around the end of the 1970s. The incidence fell to 29 cases/100,000 in 1985, which indicates that the Faroe Islands are still a high incidence area. A total of 203 cases of meningococcal disease were recorded during the period 1978-1985 with 11 deaths (lethality rate 5.4%). After rifampicin was introduced in 1981 as prophylactic treatment against secondary cases, 1,892 persons were treated with this agent and none of these appeared in the study population. Before rifampicin prophylaxis was introduced, the number of cases were distributed with an evenly increasing incidence in the capital and in the provinces. Following the introduction of rifampicin as prophylactic agent, a fall in the incidence in both areas was observed. This fall was more pronounced in the capital, where the number of prescribed prophylactic doses per case of meningococcal disease was higher than in the province.

Adolescent↗
PubMed1988

Complement C3d,g/Epstein-Barr virus receptor density on human B-lymphocytes estimated by immunoenzymatic assay and immunocytochemistry.

The density of the C3d,g/Epstein-Barr virus receptor (CR2) on human mononuclear cells (MNC) isolated from CPD stabilized blood, was determined by comparing the concentration of CR2 antigen in extracts from Raji cells, with a known receptor density, with extracts of MNC. The concentration of CR2 was determined by a sandwich ELISA using two mutually non-inhibiting monoclonal anti CR2 antibodies (HB5 and OKB7). The percentage of CR2+ MNC was determined by an immunocytochemical staining method. Analysis of MNC from 20 healthy donors, revealed that the density of CR2 molecules varied from 3,600-7,700 on CR2+ cells, and that the percentage of CR2+ MNC had a mean of 13%.

B-Lymphocytes↗
PubMed1988

Screening for complement deficiencies in patients surviving from epidemic meningococcal disease.

Sera from 132 patients surviving from meningococcal disease during the high-endemic period 1 January 1980 to 31 December 1984 on the Faroe Islands were screened for deficiencies of the complement (C) system by measuring hemolytic complement function in serum. Samples from 12 patients with reduced C function were further investigated by immunochemical quantification of individual C proteins. One patients was identified with C3-deficiency (C3-concentration 6% of normal) due to the presence of C3 nephritic factor (C3NeF) in serum. In addition, eight patients had minor aberrations in one or several complement proteins. It is concluded, that C deficiency is not an important risk factor during epidemics of meningococcal disease. The C3NeF activity could not be absorbed with Neisseria meningitidis group B, type 15, indicating absence of crossreactivity between neisserial antigens and C3NeF.

Complement C3 Nephritic Factor↗
PubMed1987

Influence of processing by erythrocyte C3b/C4b receptors (CR1) on binding of immune complexes to Raji cells and polymorphonuclear granulocytes.

The binding of 125I-labelled bovine serum albumin (BSA)-anti-BSA immune complexes (IC) to Raji cells and polymorphonuclear (PMN) cells in vitro was studied. The IC were reacted for 1 h at 37 degrees C with normal human serum (NHS) diluted 1:2 in the presence or absence of human erythrocytes (E) before presentation for Raji cells or PMN cells. The IC showed a two to three fold increased binding to C3d, g receptors (CR2) on Raji cells, when E-CR1 had been present during the reaction with NHS, compared to IC similarly reacted with NHS only. Blocking of the E-CR1 by a polyclonal anti-CR1 antibody reduced the subsequent binding of IC to Raji cells to the same level as that obtained with IC reacted with serum only. Binding to PMN granulocytes of IC reacted with NHS in the presence of E-CR1 showed a 60% reduction compared to the binding of IC reacted with NHS only. It is concluded that interaction of complement-reacted IC with CR1 on erythrocytes leads to a more efficient generation of CR2-binding C3d, g-containing IC with reduced reactivity to PMN cells.

Animals↗
PubMed1987

Screening for complement deficiencies in unselected patients with meningitis.

Two hundred and nine patients consecutively admitted to hospital with a tentative diagnosis of meningitis were screened for complement deficiency by measuring classical and alternative pathway serum haemolytic complement activity and the plasma concentration of C3d. Abnormal test results were followed up by quantitative immunochemical measurements of individual complement components. No patients with homozygous complement deficiency were found in our material. One patient with pneumococcal meningitis with probable heterozygous C2-deficiency was identified. Patients with purulent meningitis of various etiologies or meningococcal disease had significantly increased plasma C3d concentration at admission compared to patients with serous meningitis or without meningitis. Furthermore, increased plasma level of C3d at admission in patients with purulent meningitis or meningococcal disease was associated with an increased lethality. Our findings do not support the hypothesis that complement deficiency is commonly associated with sporadically occurring meningococcal disease or purulent meningitis.

Adolescent↗
PubMed1986

A family with complement factor I deficiency.

A family with inherited factor I deficiency is described. The proband was a 19-year-old Caucasian female with one episode of meningococcal meningitis and one episode of suspected septicaemia of unknown cause. Two obligate and two probable heterozygotes with factor I levels below the lower limit of the reference range were identified. None of these exhibited increased susceptibility to infectious diseases. The inheritance was autosomal codominant. In addition, molecular heterogeneity of factor H in plasma from the proband but not from any other family members was demonstrated by crossed immunoelectrophoresis. The migration of factor H component of fast electrophoretic mobility was retarded by antibodies to C3c and C3d, suggesting the presence of a fluid-phase complex between factor H and excess C3b generated by the uncontrolled activity of the amplification loop.

Adult↗
PubMed1984

Factor I deficiency and C3 nephritic factor: immunochemical findings and association with Neisseria meningitidis infection in two patients.

The complement system was examined in two patients with systemic Neisseria meningitidis infections, both of whom had reduced or nondetectable CH50 as analysed by both pathways. C3 measured by conventional technique revealed 19% anti-C3c-reactive protein in the plasma of patient 1 and 3% in patient 2. Patient 1 had circulating C3b but no detectable C3c, C3d, or C4d, whereas patient 2 had normal levels of C3c and C4d and strongly elevated levels of C3d. Factor B analysis revealed no demonstrable native factor B and small amounts of Bb in patient 1 and normal concentration of native factor B plus trace amounts of Bb in patient 2. The depletion of C3 in both patients was due to uncontrolled activation caused by complete factor I deficiency (patient 1) and circulating C3 nephritic factor (patient 2). Both parents of patient 1 had factor I concentrations below (mean-2 SD) that seen in normal healthy individuals (n = 20). Circulating immune complexes (IC) were demonstrated in patient 1 only, whereas serum from both patients had strongly reduced capacity to solubilize preformed IC.

Adolescent↗
PubMed1984

In vitro investigations of human immunoglobulin preparations: Fc-receptor reactivity and complement consumption.

The complement consuming activity and monocyte Fc-receptor (FcR) binding of some commercial IgG-preparations for intravenous (i.v.) and intramuscular (i.m.) use was investigated. A pepsin-treated IgG-preparation for i.v. use exhibited no detectable complement consuming activity and impaired FcR binding, whereas an unmodified IgG preparation had no detectable complement consuming activity, but retained full FcR binding. A preparation prepared by PEG-precipitation and ion-exchange chromatography exhibited low complement consuming activity as well as good FcR binding. Three preparations for i.m. use showed moderate to strong complement consuming activity, whereas only one of these preparations retained full FcR binding.

Complement Activation↗
PubMed1983

Simultaneous quantitation of free haptoglobin and haemoglobin-haptoglobin (HbHp) complexes by double-decker rocket immunoelectrophoresis.

Existing immunochemical methods for haptoglobin (Hp) determination are incapable of distinguishing between free haptoglobin and haemoglobin-haptoglobin (HbHp) complexes. A one-dimensional double-decker rocket immunoelectrophoretic method (DD-RIE) for simultaneous quantitation of free Hp and Hp bound as HbHp complexes was therefore developed. The DD-RIE can be used for quantitative in vitro studies of the Hb-Hp interactions, for quantitation of Hp's Hb binding capacity and for investigations of haemolytic episodes in patients. The clinical value of the method is illustrated by an investigation of a patient with a gradual accumulation of HbHp complexes in plasma, a steady rise in total Hp and a fall in free Hp during haemolysis. A proposed receptor-mediated clearance of the complexes by the reticuloendothelial system (RES) could not be substantiated, as HbHp receptors were not demonstrable on human blood monocytes.

Haptoglobins↗