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Biomedical subjects

A Rødgaard

Publications and source records attributed to A Rødgaard.

5 recordsLinked to original sources
PubMed1992

Levels of complement receptor type one (CR1, CD35) on erythrocytes, circulating immune complexes and complement C3 split products C3d and C3c are not changed by short-term physical exercise or training.

The effect of heavy short-term physical exercise on the levels of complement receptor type one (CR1, CD35) on erythrocytes, the concentrations of circulating immune complexes (IC), and the complement C3 split products C3c and C3d were examined in young healthy males. Fourteen untrained volunteers underwent a 60-min bicycle exercise test at 75% of maximal oxygen uptake (VO2max). Six of the volunteers were exercised twice with an interval of at least one month. Before the second bicycle test they received oral indomethacin. With an interval of at least 1 week, 6 also went through a 60-min back-muscle exercise at up to 30% of VO2max. Blood samples were collected before and during the last few minutes of exercise as well as 2 h and 24 h afterwards. The same parameters were examined once in 29 highly trained racing cyclists. There were no consistent or significant exercise-induced changes in the levels of erythrocyte CR1, circulating IC, C3c nor C3d as measured by an enzyme-linked immunosorbent assay, polyethylene glycol precipitation complement consumption method, and by intermediate gel rocket immunoelectrophoresis, respectively. Neither did these parameters differ from controls in the highly trained group. The results indicate that CR1 on erythrocytes, circulating immune complexes and complement cleavage products C3c and C3d in healthy subjects remain unaffected by short-term heavy physical activity and training.

Adult↗
PubMed1991

Complement receptor type 1 (CR1, CD35) expression on peripheral T lymphocytes: both CD4- and CD8-positive cells express CR1.

T lymphocytes from 42 healthy blood donors were examined for expression of CR1 on the cell surface using a fluorescence-activated cell sorter. The fraction of CR1-positive T lymphocytes varied in the range from 1 to 8% (median 2.4%). The CR1-positive T lymphocytes constituted a homogeneous group of cells regarding both size and granulation; they seemed to be larger and more granulated than the average T lymphocytes. The CR1-expressing T lymphocytes were found both in the CD4- and in the CD8-positive subpopulations of T lymphocytes, and although the CD4-positive cells expressed CR1 with a slightly higher percentage than did the CD8-positive cells, this difference was not significant. The number of CR1-positive T lymphocytes did not correlate with the level of CR1 on erythrocytes. The presence of CR1 on a small T lymphocyte population suggests that CR1 on T lymphocytes might play a role in the immune regulation.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Acetylcholine receptor antibody in myasthenia gravis: predominance of IgG subclasses 1 and 3.

The concentrations of IgG subclass antibodies (Ab) to acetylcholine receptor (AchR) were quantified in 36 patients with myasthenia gravis (MG) treated with pyridostigmine only, and in eight patients who underwent thymectomy, using an IgG subclass-specific immunoprecipitation assay. IgG1, IgG2, IgG3, and IgG4 subclass Ab to AchR were present in 100%, 33%, 64% and 39% of the pyridostigmine-treated patients, respectively. The concentration of IgG1 Ab increased significantly with disease severity as graded by the Osserman-Genkins classification (rs = 0.37, P less than 0.05). IgG1 and IgG3 subclass protein concentrations were significantly higher (P less than 0.0003) in the 36 pyridostigmine-treated MG patients than in 44 age- and sex-matched healthy subjects. Thymectomy induced an appreciable reduction in anti-AchR IgG1 concentration in two patients, whereas six patients showed no changes in Ab to AchR. The results support the hypothesis that binding of anti-AchR IgG1 and IgG3 on AchR in the neuromuscular junction followed by complement-mediated cell lysis or phagocytosis, may play a role in the pathogenesis of MG.

Humans↗
PubMed1985

A triple antibody assay for the quantitation of plasma IgG subclass antibodies to acetylcholine receptors in patients with myasthenia gravis.

Monoclonal anti-human IgG subclass antibodies have been used in an immunoprecipitation assay for the determination of anti-acetylcholine receptor IgG subclasses in plasma from patients with myasthenia gravis. Solubilized acetylcholine receptors labelled with 125I-alpha-bungarotoxin were incubated with patient plasma. Monoclonal mouse antibodies to human IgG subclasses 1-4 were added to the incubation and finally precipitated with anti-mouse IgG antibody. A maximal IgG subclass precipitation of 62-76% was determined with 125I-labelled myeloma IgG subclasses 1-4 added to normal human plasma. The anti-IgG subclass antibodies were added in excess which ensured that the precipitation of IgG2, IgG3 or IgG4 were unchanged, and that of IgG1 was only reduced by 17%, when the plasma IgG concentration was increased by a factor of two. The anti-IgG subclass antibodies were highly specific for their complementary subclasses. Determination of the IgG subclass of the anti-acetylcholine receptor antibodies from 8 patients with myasthenia gravis showed that IgG1 and IgG3 antibodies are predominant. This may support the hypothesis that complement mediated lysis of the neuromuscular end-plate plays a pathogenetic role in myasthenia gravis.

Antibodies, Monoclonal↗