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Biomedical subjects

O Bruserud

Publications and source records attributed to O Bruserud.

101 records · Page 6Linked to original sources
PubMed1985

HLA control of the proliferative T lymphocyte response to antigenic determinants on mumps virus. Studies of healthy individuals and patients with type 1 diabetes.

The proliferative T lymphocyte responses to two different mumps antigen preparations, S (nucleocapsid) and V (viral envelope), were characterized. Eight patients with Type 1 (insulin-dependent) diabetes mellitus were all found to be responders to S and V mumps antigen. Among the 64 healthy individuals, 52 were classified as responders to the S antigen and 50 responders to the V antigen. No difference was found between T lymphocytes from Type 1 diabetic patients and those from healthy individuals as regards the effect of indomethacin on the mumps-specific response. The majority of the mumps-specific T lymphocytes seemed to be restricted by epitopes on the HLA-DR molecules. The frequency of mumps antigen-reactive T lymphocytes (ARTL) was found to be low when the response was restricted by DR3-associated elements, and high when it was restricted by DR4-associated elements, compared to the frequency of ARTL when other DR-associated elements restricted the mumps-specific response. For the majority of the individuals tested, the DR-associated hypo- and hyper-responsiveness was found with both the S and the V mumps antigens.

Antibodies, Monoclonal↗
PubMed1985

T lymphocyte responses to Coxsackie B4 and mumps virus. I. Influence of HLA-DR restriction elements.

The proliferative T lymphocyte responses to Coxsackie B4-, mumps- and varicella-zoster viral antigens were characterized. No significant difference in responsiveness was found between healthy individuals and patients with Type 1 (insulin-dependent) diabetes mellitus. Theophyllamine and verapamil decreased antigen-stimulated proliferation, whereas indomethacin in physiologic concentrations (1 microgram/ml) slightly increased proliferation. A major part of the response seemed to be restricted by HLA-DR molecules. Furthermore, for the mumps antigen the DR3- and DR4-determinants which are associated with Type 1 diabetes, seemed to have a different regulatory function on the T lymphocyte response in that an increased frequency of low responders was found among DR3 positive individuals and an increased frequency of high responders among DR4 positives.

Aminophylline↗
PubMed1985

T lymphocyte responses to Coxsackie B4 and mumps virus. II. Immunoregulation by HLA-DR3 and -DR4 associated restriction elements.

A major part of the T lymphocyte response to mumps and Coxsackie B4 virus appears to be restricted by HLA-DR associated restriction elements. This was further corroborated in inhibition experiments using monoclonal antibodies reactive with different HLA class II molecules. Only antibodies reactive with DR molecules significantly inhibited the response. The frequencies of DR restricted antigen-reactive T lymphocytes (ARTL) to mumps and Coxsackie B4 virus were then investigated, using a limiting dilution assay. A decreased frequency of DR3 restricted ARTL to mumps and Coxsackie B4 was found compared to ARTL restricted by other DR associated elements. In contrast, an increased frequency of DR4 restricted ARTL to mumps and Coxsackie B4 was found. The results were similar for healthy individuals and Type 1 diabetic patients. No correlation was found between DR restriction elements and the frequencies of ARTL to varicella-zoster or PPD. The studies indicate that HLA-DR3 and DR4, which are associated with Type 1 diabetes, have a different regulatory function on the proliferative T lymphocyte response to mumps and Coxsackie B4.

Antibodies, Monoclonal↗
PubMed1984

Production of interleukin 2 containing growth medium for cloning of human T lymphocytes.

Culture conditions which would enhance production of interleukin 2 (IL-2) from PHA-stimulated peripheral blood mononuclear cells (PBM) were studied. One thousand rads. irradiation of the cells was found to alter the kinetics and to increase the production of IL-2. Addition of indomethacin or irradiated EBV-transformed B lymphocytes to the cultures, removal of adherent cells, and 18 h preincubation of the cells before PHA stimulation had an additive enhancing effect on the IL-2 production. Following these studies a simple and efficient method producing IL-2 for cloning of human T cells was developed.

B-Lymphocytes↗
PubMed1984

The effect of theophyllamine on T-lymphocyte activation in vitro.

Theophyllamine in similar concentrations as the therapeutic serum level was found to inhibit the proliferative response in mixed lymphocyte cultures (MLC) and cultures stimulated with purified protein derivative of tuberculin (PPD). Theophyllamine inhibited interleukin 2 (IL-2) production of lymphocytes stimulated with phytohemaglutinin (PHA) and IL-2-dependent growth of T-cell lines, but had no effect on PPD pulsing of antigen-presenting cells.

Aminophylline↗
PubMed1983

Identification of four SB antigens by cloned cells. Population studies of Norwegians.

By priming in vitro with allogeneic HLA-DR compatible and also HLA-A,B mostly compatible lymphoid cells, PLT cells resulted in recognizing a group of non D/DR allelic antigens provisionally named K, L, M and N. To improve discrimination these bulk primed typing reagents were cloned and expanded. By typing of previously SB typed lymphoblastoid B cell lines (LCL) the provisional specificities could be identified as SB1, 4, 3 and 2, respectively. Typing of 186 unrelated Norwegians gave the following gene frequences: SB1: 0.05, SB2: 0.16, SB3: 0.13, SB4: 0.42 and SB blank: 0.24. No triplets were found, the calculated gene frequencies fit with Hardy-Weinberg equilibrium, and typing of a B-DR recombinant family confirmed that the SB locus is situated centromeric to B. Associations between SB and A, B, DR antigens in the same material were generally weak, the most significant associations found were between SB1-DR3 and SB4-DR2.

B-Lymphocytes↗
PubMedDate not supplied

Hematopoietic growth factors in patients receiving intensive chemotherapy for malignant disorders: studies of granulocyte-colony stimulating factor (G-CSF), granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-3 (IL-3) and Flt-3 ligand (Flt3L).

The levels of hematopoietic growth factors in patients receiving intensive chemotherapy for malignant disorders were investigated using a variety of approaches. Firstly, serum levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF and Flt3-ligand (Flt3L) were examined in acute leukemia patients with treatment-induced cytopenia and complicating bacterial infections. Increased serum levels of both G-CSF and Flt3-ligand (Flt3L) were detected when these patients developed therapy-induced leukopenia, whereas GM-CSF levels were low or undetectable. Development of complicating bacterial infections then increased the serum levels of both G- and GM-CSF, and the Flt3L levels remained high during the infections. Secondly, release of growth factors was characterized for clonogenic T cells that remained in the circulation of acute leukemia patients with chemotherapy-induced cytopenia. CD4(+) and CD8(+) T cells from these patients released high levels of GM-CSF, relatively low levels of IL-3 secretion having been detected, and only a minority of the clones released detectable amounts of Flt3L. Thus, circulating T cells may contribute to the high systemic growth factor levels in cytopenic patients. Thirdly, plasma levels of GM-CSF and interleukin-3 (IL-3) were examined in patients with malignant disorders who received chemotherapy plus G-CSF for stem cell mobilization. Increased levels of GM-CSF and Flt3L were detected both in the patients' plasma and in the stem cell grafts. Despite the increased growth factor levels in neutropenic patients with complicating infections, the occurrence of febrile neutropenia did not have a major impact on normal hematopoietic reconstitution (i.e. duration of treatment-induced neutropenia) after intensive chemotherapy for acute myelogenous leukemia.

Adolescent↗