Search PubMed⌕ Search

Biomedical subjects

K Bendtzen

Publications and source records attributed to K Bendtzen.

At least 289 records · Page 16Linked to original sources
PubMed1986

Proliferation induced by Plasmodium falciparum antigen and interleukin-2 production by lymphocytes isolated from malaria-immune individuals.

Affinity-purified Plasmodium falciparum soluble antigens (SPAg) isolated from in vitro cultures of the parasite were shown to be relatively free of nonspecific polyclonal activators. To determine the presence of lymphocytes with specificity against SPAg in the peripheral blood of malaria-immune individuals, the proliferative response and the interleukin-2 (IL-2) production of SPAg-activated mononuclear cells (MNCs) from individuals unexposed, sensitized, and immune to malaria were measured. It was found that MNC isolated from malaria-immune individuals proliferated in response to SPAg and that this activation resulted in measurable IL-2 production in 5 of 10 MNC cultures. MNC isolates from most unexposed individuals did not respond to SPAg. To establish which cells responded to SPAg, different subpopulations of MNCs were tested. Only T helper cells were found to respond, and they responded only when cocultured with monocytes. The finding of parasite-specific T helper cells in the blood of malaria-immune individuals and the fact that some of these cells were able to produce IL-2 in vitro support the hypothesis that in malaria the cellular part of the protective immune response is initiated by immune T cells. These cells may activate nonspecific effector cells (i.e., macrophages) that eliminate the parasite.

Adult↗
PubMed1986

Low concentrations of interleukin-1 stimulate and high concentrations inhibit insulin release from isolated rat islets of Langerhans.

Isolated rat islets were incubated either with crude, affinity-purified or recombinant human interleukin-1 for 1 to 6 days. A significant (20-60%) increase of insulin release was observed at low concentrations of all three interleukin-1-containing preparations. In contrast, higher concentrations dose-dependently inhibited the insulin release. The increased insulin secretion occurred at concentrations below those necessary to augment the mitogen response to phytohaemagglutinin of murine thymocytes in vitro. These doses (0.05-0.5 U/ml) correspond to 0.2-2 ng of recombinant interleukin-1 per ml, equal to approximately 0.01-0.1 pmol/ml. In doses of 0.6-1.8 U/ml affinity-purified interleukin-1 significantly increased the islet insulin content per ng of DNA, indicating a stimulation of insulin-biosynthesis. The data support the concept that low concentrations of interleukin-1 may play a role in priming the physiological secretion of insulin.

Animals↗
PubMed1986

Blood mononuclear cells in patients with primary Sjögren's syndrome: production of interleukins, enumeration of interleukin-2 receptors, and DNA synthesis.

Disturbed immunoregulation is considered an essential feature of the pathogenesis in primary Sjögren's syndrome (primary SS). After in vitro stimulation we investigated the interleukin-1 production by blood monocytes, interleukin-2 production by blood T-lymphocytes, the number of IL-2 receptor-bearing blood T-lymphocytes and the blood lymphocyte DNA synthesis in 6 consecutive female patients with primary SS and in 6 female controls. In the patient group we found all the parameters examined within a wider range as compared to the controls. The three patients with reduced interleukin-2 production and low proliferative responses were exclusively characterized by elevated plasma-IgG concentration, positive antinuclear antibodies and rheumatoid factor, and by having circulating immune complexes.

DNA↗
PubMed1985

Interleukin-1-like activities in synovial fluids of patients with rheumatoid arthritis and traumatic synovitis.

Interleukin-1 (Il-1)-like activity in biological fluids was measured by their ability to rectify the Il-1-dependent lymphokine production of highly purified T lymphocytes to a recall antigen. Il-1-like activity was found in 9 of 11 synovial fluid (SF) specimens from patients with rheumatoid arthritis (RA) but only in 2 of 11 paired RA sera. In traumatic synovitis, low Il-1-like activity was recorded in 5 of 9 SF specimens, and a similar low activity was found in sera of 4 of these patients. The Il-1-like activity was partly absorbed by an anti-Il-1 antibody. The presence of Il-1 in the SF of patients with RA suggests in vivo activation of monocytes/macrophages.

Adsorption↗
PubMed1985

Interleukins.

Explore the source record for details and available documents.

Cell Division↗
PubMed1985

Effects of cyclic GMP-agonists on cyclosporin-induced suppression of human lymphokine production.

Cyclosporin (Cs) inhibits the elaboration of the lymphokine leukocyte migration inhibitory factor (LIF) from human blood mononuclear cells (MNC) stimulated with recall antigen. This inhibition was counteracted by 3 X 10(-5) M dibutyryl-cyclic GMP and 8-bromo-cyclic GMP and by the cyclic GMP-agonists, sodium nitroprusside (NaNPr), ascorbic acid (As A), sodium azide (NaN3) and carbacholine. Using 5 X 10(-5) M NaNPr, 1 X 10(-3) M NaN3, or 3 X 10(-3) M As A, 25-50-, 4-8- and 2-3-fold elevations of MNC and T-lymphocyte cyclic GMP-levels were obtained independently of the presence of Cs. NaNPr was the most potent of these three cyclic GMP-agonists in counteracting the effect of Cs. The results indicate that intracellular cyclic GMP is a major factor involved in the reversal of Cs-induced inhibition of LIF-production. None of the cyclic GMP-analogues or -agonists by themselves possessed Interleukin 1-like activity, measured by their ability to induce LIF-production by macrophage-depleted T-lymphocytes challenged by recall antigen.

Adult↗
PubMed1985

Inhibitory effect of cyclosporin A on histamine release from human leukocytes and rat mast cells.

The influence of cyclosporin A (CyA) on human basophil histamine release induced in vitro by specific antigen, anti-IgE, calcium ionophore A23187, or concanavalin A (Con A) was studied. CyA inhibited the release induced by these four stimulators. It is suggested that the drug acts directly on the target cell, since similar effect was obtained with isolated peritoneal rat mast cells. The basophil histamine release was not changed by a non-immunosuppressive cyclosporin derivate.

Animals↗
PubMed1985

Cytokines cause functional and structural damage to isolated islets of Langerhans.

Cytokines are soluble, antigen non-specific, non-immunoglobulin mediators produced and secreted by blood mononuclear cells interacting in the cellular immune-response. To test the possibility that cytokines participate in the autoimmune destruction of the pancreatic beta-cells leading to insulin-dependent diabetes mellitus, isolated human or rat islets of Langerhans were incubated for 7 days with cytokine-rich, cell-free supernatants of blood mononuclear cells from healthy human donors stimulated with or without purified protein derivative of tuberculin or phytohaemagglutinin. Glucose stimulated insulin-release, and contents of insulin and glucagon in islets incubated with cytokine-rich supernatants were markedly reduced. This impairment of islet function was due to a cytotoxic effect of cytokine-rich supernatants as judged by disintegration of normal light-microscopic morphology.

Animals↗
PubMed1984

An unusual case of multiple malignancy in an adult.

An adult female is described who, during a clinical course of 25 years, presented malignant tumors of the rectum, breast, uterus and colon. Cytostatics were never administered. Lymphocyte subsets, a variety of lymphocyte and mononuclear cell stimulation assays with mitogens and antigens, DNA repair tests and activity of natural killer cells were normal. Serum leukocytic interleukin-1 activity was slightly elevated. Sister chromatid exchange frequency in peripheral lymphocytes was below the normal range. An explanation for the development of 4 primary malignant neoplasms was not found.

Breast Neoplasms↗
PubMed1984

Influence of endotoxin on production of leucocyte migration inhibition factor. Part I.

Commercial reagents are often contaminated with endotoxins in concentrations which may affect biological immunoassays. The endotoxin lipopolysaccharide from E. coli 026:B6, at concentrations at and above 5 X 10(-9) g/ml induces mononuclear cells to produce the lymphokine leucocyte migration inhibition factor (LIF). However, lipopolysaccharide at concentrations at or above 5 X 10(-8) inhibit leucocyte migration making it impossible to measure the effect of LIF. Standardization of endotoxin content during production and assay of LIF is needed, in order to reduce the variability of the results.

Adult↗
PubMed1984

Role of monocytes/macrophages and interleukin 1 in antigen-induced human lymphokine production.

The monocyte/macrophage (M phi)-dependency for antigen-induced production of the lymphokine, leukocyte migration inhibitory factor (LIF), was investigated using a M phi pulse-exposure technique. M phi-depleted, purified T lymphocytes did not elaborate LIF in response to the recall antigen, tuberculin (PPD). Addition of M phi's pulsed with PPD rectified the response. Exposure of the M phi's down to 3 min, even at 0 degree C, was efficacious. PPD-exposed M phi's, either killed or rendered incapable of protein synthesis, failed to activate the T cells. However, PPD-exposed, killed M phi's triggered LIF production if exogenous interleukin 1 (IL-1) was provided. We suggest that M phi "presentation" of antigen in this test system is a passive albeit necessary, process; the requirement for M phi metabolism being confined to the elaboration of IL-1. Judged by the results of kinetic experiments, the latter stimulus appears to be mediated most effectively from 2 to 4 hr after antigenic challenge.

Adult↗
PubMed1984

EGNA-specific LIF production of human lymphocyte subsets.

Using the indirect leukocyte migration inhibition technique T cells have been identified as being responsible for Epstein-Barr virus nuclear antigen-induced specific leukocyte migration inhibitory factor production. The response was dependent on the presence of macrophages or their product, T-lymphocyte activating factor.

Antigens, Viral↗
PubMed1984

Production of leukocyte migration inhibitory factor (LIF) in human lymphocyte subsets exposed to polyclonal activators.

Lymphocyte subsets separated on the basis of nylon-wool adherence and E and EA rosetting, and characterized for the presence of esterase-positive phagocytic cells were investigated for production of leukocyte migration inhibitory factor (LIF) in response to polyclonal T- and B-cell activators, PHA, ConA, PWM, and Epstein-Barr virus (EBV). In the nylon-passed population only the high avidity E+EA+ cells responded to ConA, PHA-induced LIF production in all E-rosetting subsets. The nylon-adherent E+ subset, which contains activated T cells, produced LIF spontaneously. B cells produced LIF when exposed to PWM or uv-inactivated EBV. In accordance with the known T-cell dependence of PWM activation, LIF was detected only in supernatants of reconstituted populations containing both B and T cells. In contrast, uv-inactivated EBV, devoid of transforming potential, elicited LIF production in the pure B-cell population. LIF production in response to polyclonal activators seemed to be independent of accessory cells since reconstitution with autologous macrophages or semipurified monokine, high-molecular-weight Interleukin 1 (IL-1), did not alter the results.

B-Lymphocytes↗