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Biomedical subjects

A Perl

Publications and source records attributed to A Perl.

At least 73 records · Page 4Linked to original sources
PubMed1986

Quantitative determination of anti-A-dependent cytotoxicity of human peripheral blood monocytes.

A simple test is suggested for the quantitative measurement of the cytotoxic activity of human peripheral monocytes. Adherent cells are separated from non-adherent cells in the wells of the microtiter plates, thus tedious resuspension of effector cells can be omitted. Effector cell number is accurately determined by isotope labelling. Maximum of cytotoxic activity is measured in the enzyme-like kinetic model of cytotoxicity as a function of target cell number. It was found that 34.2-51.2% of unseparated peripheral blood mononuclear cells (PBMC) were adherent. More than 80% of these were shown to be monocytes by monoclonal antibodies and alpha-naphthyl acetate esterase (ANAE) staining. Depletion of SRBC rosette forming cells prior to adherence (PBMC, E-) resulted in enrichment of adherent cells (61.3-82.8%), which were exclusively monocytes. Cytotoxic activity of both adherent populations (PBMC and PBMC, E-) for human red blood cells sensitized with anti-A was determined experimentally and also extrapolated by using the Michaelis-Menten equation. It was estimated that one monocyte was able to lyse more than 4 erythrocytes.

ABO Blood-Group System↗
PubMed1986

Depressed lectin-dependent and enhanced antibody-dependent cell-mediated cytotoxicity in patients with stage I cancer of the larynx.

Lectin-dependent cell-mediated cytotoxicity (LDCC) of peripheral blood mononuclear cells (PBMC) from patients with stage I cancer of the larynx (LC) was evaluated using human adherent 3H-TdR-prelabeled HEp-2 carcinoma cells as targets at 50:1 effector-target ratio with 25 micrograms/ml concanavalin A (Con A) in a 24-hour assay. Under these conditions, but without Con A, no considerable natural cell-mediated cytotoxicity (NCMC) was performed by PBMC either from control or from LC donors. Depressed levels of LDCC, but augmented ADCC to chicken red blood cells were detected in LC patients. Natural killer activity to K562 targets was not different from that of control subjects. In parallel studies, normal Con A-induced blastogenesis and B cell counts, low T, and active T cell counts, as well as high Leu-11a+ cell counts were detected in patients with LC. The relationship between depressed LDCC and low T, and active T cell counts, and enhanced ADCC and high Leu-11a+ cell counts is suggested in stage I LC patients.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1986

Independence of depressed lectin-dependent cell-mediated cytotoxicity from interleukin 2 production in patients with systemic lupus erythematosus.

The relationship of lectin-dependent cell-mediated cytotoxicity (LDCC) to interleukin-2 (IL-2) production was studied in healthy subjects and in patients with systemic lupus erythematosus (SLE). Profoundly depressed levels of LDCC were elicited by peripheral blood mononuclear cells (PBMC) from nine patients with active SLE in comparison to LDCC from seven controls, and eleven inactive SLE donors, using 3H-TdR-prelabelled adherent HEP-2 cells as targets in a 24 h assay with 25 micrograms/ml Con A. In parallel experiments, no individual correlation was found between LDCC activity and IL-2 production for healthy or SLE subjects. Further, no major differences were detected in IL-2 release when the three groups of donors were compared, a tendency observed at the Con A doses (5 and 25 micrograms/ml) and incubation times (24, 48, and 72 h) used to induce IL-2 production. In additional studies, impaired Con A-induced blastogenesis was noted for PBMC from active SLE patients in comparison to the PBMC from the controls or patients with inactive SLE. While strong individual correlation was obtained between blastogenesis and IL-2 secretion in controls and patients with inactive SLE, no such relationship was found in patients with active SLE. While addition of exogenous IL-2 to the cytotoxicity assay considerably enhanced LDCC by healthy donors it failed to improve LDCC by patients with active SLE. These data suggest that depressed LDCC and Con A-induced blastogenesis of patients with active SLE may not be related to impaired IL-2 production but rather to an inherent dysfunction of the effector lymphocytes, including their unresponsiveness to IL-2.

Concanavalin A↗
PubMed1986

Lectin-dependent cell-mediated cytotoxicity and blastogenesis by large granular-enriched and depleted lymphocytes.

The role of larger granular-enriched and depleted lymphocytes was studied in lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. LDCC was evaluated by detachment from the monolayer of 3H-thymidine-prelabelled HEp-2 cells in a 24 h assay at effector-target cell ratios of 25:1 and 50:1 in the presence of 25 micrograms/ml concanavalin A (Con A). Under the aforementioned conditions but in the absence of Con A natural cell-mediated cytotoxicity (NCMC) was not found. However, cytotoxicity was significantly augmented in the presence of Con A (= LDCC) using human peripheral blood mononuclear cells (PBMC) as effectors. Large granular lymphocytes (LGL), which show high natural killer (NK) activity to K 562 target cells, failed to be cytotoxic against HEp-2 targets similar to large granular depleted lymphocytes (LGL-DL). On the other hand, LGL caused only a slight LDCC; whilst LGL-DL induced strong LDCC activity towards HEp-2 targets. In comparison to LDCC using LGL-DL as effector cells, LGL and LGL-DL mixed at a ratio of 1:2, and added to target cells, had no major effect on LDCC, while a lower level of LDCC was observed at LGL/LGL-DL ratios of 1:1, and 2:1, suggesting the dilution of LGL-DL, potential effectors of LDCC to HEp-2 cells, rather than a specific regulatory role of LGL in LDCC. In parallel studies, the proliferation of LGL-DL in response to Con A was less than that observed with PBMC or LGL. The response could be restored by replacing half of LGL-DL per culture with an equal number of LGL, or by the addition of 10% monocytes. Significant functional differences between LGL and LGL-DL in LDCC as well as in Con A-induced blastogenesis are suggested.

Cell Line↗
PubMed1985

Contrasting effects of RNA and protein synthesis blocking on natural and lectin-dependent cell-mediated cytotoxicity against adherent HEp-2 cells.

In this study, earlier observations concerning the independence of both natural (NCMC) and lectin-dependent cell-mediated cytotoxicity (LDCC) from DNA synthesis have been confirmed. In addition, blocking of RNA synthesis by actinomycin D and of protein synthesis, reversibly by puromycin (PM) and irreversibly by emetine (EM) had different effects on NCMC and LDCC against 3H-thymidine-prelabeled HEp-2 target cells. Similarly to the Con A-induced proliferation of lymphocytes, LDCC activity was also inhibited by blocking of RNA and protein synthesis. NCMC to HEp-2 target cells was not affected by blocking of RNA synthesis, while both PM and EM strongly enhanced NCMC activity.

Cell Adhesion↗
PubMed1985

Thoracoabdominal motion during hypercapnia, hypoxia, and exercise.

We measured, in 11 healthy volunteers, the contributions of rib cage and abdomen--diaphragm compartments to increased ventilation caused by hypercapnia, hypoxia, and exercise to determine whether different stimuli produce similar or different patterns of ventilation with respect to the motion of rib cage and abdominal compartments. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia were induced by rebreathing methods and graded exercise performed on a treadmill, and compartmental tidal volume (VT) was measured by respiratory inductive plethysmography. For each stimulus, the wide range of VT responses among individuals was determined primarily by the range of rib cage contributions to VT, the abdominal compartment VT response slopes accounting for less of this range. There were no significant differences between hypercapnia and hypoxia in either rib cage or abdominal contributions to ventilation (for both, p less than 0.3). However, exercise rib cage and abdominal contributions to ventilation were significantly different from those during chemically driven breathing: for the rib cage compartment, p less than 0.0001 and for the abdominal compartment, p less than 0.05. Whereas, in 8 of 10 subjects the rib cage contribution to VT during exercise was similar to or exceeded that during rebreathing, in 7 of 10 subjects the abdomen-diaphragm contribution fell below that measured during both hypercapnia and hypoxia. There was a significant correlation between hypercapnia and hypoxia in the VT contribution of each compartment at equivalent levels of ventilation (rib cage, p less than 0.0001; abdomen, p less than 0.0005), but there was no significant correlation in the VT contribution of either compartment between exercise and hypercapnia or exercise and hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1985

Depressed lectin-dependent cell-mediated cytotoxicity against HEp-2 cells in patients with metastasizing solid tumour.

Lectin-dependent cell-mediated cytotoxicity (LDCC) of peripheral blood mononuclear cells (PBMC) from tumour patients was evaluated using human adherent 3H-TdR-prelabelled HEp-2 epipharynx carcinoma cells as targets at 50:1 effector-target cell ratio with 25 micrograms/ml concanavalin A (Con A) in a 24h assay. PBMC of nine patients with metastasizing solid tumour failed to exert cytotoxicity against HEp-2 targets. In contrast, increased survival (decreased detachment from the monolayer) of HEp-2 cells was observed in the presence of PBMC from tumour patients that was significantly enhanced by addition of Con A during LDCC assay.

Cell Line↗
PubMed1985

Stimulation by thymopoietin oligopeptides of lectin-dependent cell-mediated cytotoxicity in patients with systemic lupus erythematosus.

The effect of thymopoietin penta- (TP-5), tetra-(TP-4), and tripeptides (TP-3) was studied on the depressed lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 target cells by peripheral blood mononuclear cells from patients with active systemic lupus erythematosus (SLE). LDCC activity was evaluated by detachment from the monolayer of 3H-thymidine-prelabelled HEp-2 cells in the presence of concanavalin A (Con A). While 10(-5)M TP-3 moderated the depression, 10(-5) M TP-5 strongly enhanced LDCC activity in SLE patients up to the normal level. On the other hand, LDCC activity by normal donors was not influenced by TP-3 and TP-5. TP-4 had no major effect either in control or in SLE patients. In parallel experiments none of the thymopoietin peptides affected the Con A-induced suppressor activity on the blastogenesis of lymphocytes. A selective immunostimulatory effect of TP-3 and TP-5 on the generation of LDCC effector cells in patients with SLE is suggested.

Concanavalin A↗
PubMed1985

Effect of histamine-receptor blocking on human natural and lectin-dependent cell-mediated cytotoxicity against adherent HEP-2 cells.

The effect of histamine (H) and H1-, H2-receptor blocking agents was studied on natural (NCMC) and lectin-dependent cell-mediated cytotoxicity (LDCC) of peripheral blood lymphocytes (PBL) from eight healthy subjects on HEP-2 adherent human epipharynx carcinoma target cells. Cytotoxicity was measured by detachment from the monolayer of 3H-TdR-prelabelled HEp-2 cells. LDCC was evaluated in a 24 h assay with a Concanavalin A (Con A) dose of 25 micrograms/ml at 50:1 effector-target cell ratio. Under these conditions, but without Con A, considerable NCMC was not elicited by normal lymphocytes. The presence of histamine and the H2-receptor blocker cimetidine resulted in a significant NCMC to HEp-2 cells. On the contrary, histamine and cimetidine reduced LDCC. The H1-receptor blocker clemastine had no significant effect on either NCMC or LDCC to HEp-2 targets. The possible involvement of H2-receptor bearing cells in the regulation of cytotoxicity to HEp-2 cells is suggested.

Cell Adhesion↗
PubMed1984

Effector activity of OKT4+ and OKT8+ T-cell subsets in lectin-dependent cell-mediated cytotoxicity against adherent HEp-2 cells.

The role of OKT4+ and OKT8+ T-cell subsets was studied in lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. LDCC was evaluated by detachment from the monolayer of [3H]thymidine prelabeled HEp-2 cells in a 24-hr assay with a concanavalin A (Con A) dose of 25 microgram/ml at effector:target cell ratios of 5:1, 25:1, and 50:1. Under these conditions but without Con A considerable natural cell-mediated cytotoxicity (NCMC) was not elicited; however, the cytotoxicity was significantly augmented in the presence of Con A (=LDCC) by sheep erythrocyte rosette-forming T lymphocytes and by both OKT4+ and OKT8+ T-cell fractions. LDCC activity by isolated OKT8+ T cells was superior to that by OKT4+ T cells and unfractionated T lymphocytes. By contrast, addition of either OKT4+ or OKT8+ T cells together with unfractionated T lymphocytes, or OKT4+ and OKT8+ T cells mixed at ratios of 1:1, 1:2, and 2:1, to target cells did not result in major differences in comparison of LDCC activities by these mixed effector cell populations with each other or with that by unfractionated T lymphocytes. Parallel studies were carried out to determine the effect of OKT4+ and OKT8+ T-cell subsets on the Con A-induced proliferation of peripheral blood mononuclear cells (PBMC). While OKT8+ T cells inhibited the mitogenic response to Con A, OKT4+ T lymphocytes had no major effect. A higher responsiveness of the OKT8+ to OKT4+ T-cell subset in LDCC to HEp-2 targets and in Con A-induced lymphocyte proliferation is suggested.

Antibodies, Monoclonal↗
PubMed1984

Ketoconazole in vitro inhibits mitogen-induced blastogenesis, antibody-dependent cellular cytotoxicity, natural killer activity and random migration of human leukocytes.

Ketoconazole at concentrations of 1-10 micrograms/ml dose dependently inhibits mitogen-induced blastogenesis, antibody-dependent and spontaneous cytotoxic (natural killer) activity of human lymphocytes and random migration of human leukocytes. Lectin-dependent cytotoxic activity is not affected by the drug.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1984

Depressed effector activity of OKT4+ and OKT8+ T cell subsets in lectin-dependent cell-mediated cytotoxicity to HEP-2 cells in patients with systemic lupus erythematosus.

The role of OKT4+ and OKT8+ T cell subsets was studied in depressed lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 target cells by peripheral blood mononuclear cells (PBMC) from patients with active systemic lupus erythematosus (SLE). LDCC activity was evaluated by detachment from the monolayer of 3H-TdR-prelabelled HEp-2 cells in a 24 hr assay at 50:1 effector-target cell ratio in the presence of 25 micrograms/ml concanavalin A (Con A). Decreased levels of LDCC were performed by all studied effector cell populations of SLE patients, including both OKT4+ and OKT8+ T cell fractions. LDCC by isolated OKT8+ T cells was superior to that by OKT4+ and unfractionated T lymphocytes from all healthy and SLE subjects. This suggests that the defect of LDCC activity in SLE did not affect the inherently higher LDCC effector activity of OKT8+ to OKT4+ cells. In parallel studies a reduced proliferation of PBMC in response to Con A and failure of OKT8+ T cells to suppress Con A-induced blastogenesis was observed in patients with SLE.

Adult↗
PubMed1983

Depressed lectin-dependent cell-mediated cytotoxicity against adherent HEP-2 cells in patients with carcinoma of the uterine cervix.

Lectin-dependent cell-mediated cytotoxicity of peripheral blood mononuclear cells from patients with uterine cervix carcinoma was evaluated using human adherent 3H-TdR-prelabeled HEp-2 epipharynx carcinoma cells as targets at a 50:1 effector-target cell ratio with 25 micrograms concanavalin A/ml in a 24-h assay. Peripheral blood mononuclear cells from 13 patients with cervical carcinoma in stage IV failed to exert cytotoxicity against HEp-2 targets. In contrast, an increased survival (decreased detachment from the monolayer) of HEp-2 cells was observed in the presence of peripheral blood mononuclear cells from patients, this being significantly enhanced by addition of concanavalin A during the lectin-dependent cell-mediated cytotoxicity assay.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1983

Effect of Fc receptor blocking on human natural and lectin-dependent cell-mediated cytotoxicity against adherent HEp-2 cells.

The effect of Fc receptor (FcR) blocking by aggregated human gamma-globulin (AGG) was studied on natural (NCMC) and lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. Cytotoxicity was measured by detachment from the monolayer of [3H]TdR-prelabelled HEp-2 cells. LDCC was evaluated in a 24 h assay at 50:1 effector-target cell ratio in the presence of 25 micrograms/ml concanavalin A (Con A). Under these conditions but without Con A considerable NCMC was not elicited by normal lymphocytes. FcR blocking by AGG treatment of effector cells resulted in a significant NCMC activity to HEp-2 targets. In contrast, AGG treatment profoundly depressed LDCC. Monocyte depletion of effector cells had no major influence on the effect of AGG on NCMC and LDCC activities. An interference of FcR blocking by AGG and LDCC in response to Con A is suggested.

Cell Line↗
PubMed1983

Human lectin-dependent T cell-mediated cytotoxicity against Hep-2 cells.

A sensitive method for human lectin-dependent cell-mediated cytotoxicity (LDCC) is presented using HEp-2 adherent human epipharynx carcinoma cells as targets. Cytotoxicity was evaluated by detachment from the monolayer of 3H-TdR-prelabelled HEp-2 cells. Maximal LDCC was obtained in a 24 h assay with a Con A dose of 25 micrograms/ml for 50 : 1 effector-target cell ratio requiring only 2500 target cells per well. Testing of five different lymphocyte fractions: peripheral blood mononuclear cells (PBMC), monocyte-enriched adherent cells (AC), monocyte-depleted non-adherent cells (non-AC), T and non-T lymphocytes as effector cells from 25 normal individuals, suggests that LDCC to HEp-2 targets is mediated by T lymphocytes.

Cells, Cultured↗
PubMed1983

Characterization of the effector cells in Con A-induced cytotoxicity against HEp 2 tumour targets.

Con A-induced cytotoxic activity of human lymphocyte subpopulations obtained by cell fractionation procedures was studied in a test system using human epipharynx carcinoma cells (HEp 2) as targets. Only T lymphocytes were cytotoxic, non-T cells exerted no cytotoxic activity, but enhanced the adherence of the tumour cells. Tnon-G lymphocytes (Fc-receptor negative T cells) were more active than TG cells (Fc-receptor-positive T cells) in mediating the Con A-induced cytotoxic reaction.

Cell Line↗