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Biomedical subjects

R Lomnitzer

Publications and source records attributed to R Lomnitzer.

15 recordsLinked to original sources
PubMed1988

Isoprinosine potentiation of human peripheral blood mononuclear cell response to mitogens: kinetics and effect on expression of the IL-2 receptor and the activity of interleukin 2.

Isoprinosine, a synthetic purine derivative, enhanced the proliferative response of peripheral blood mononuclear cells to the lectin phytohaemagglutinin, and to the monoclonal antibody OKT3. The drug did not potentiate the activation of cells following oxidation by sodium periodate. Isoprinosine had no effect on the expression of receptors for interleukin-2. Increased interleukin-2 activity was detected in three out of nine supernatants from PHA activated mononuclear cells which were cultured in the presence of isoprinosine. Kinetic experiments involving addition or removal of the drug at various time intervals indicated that potentiation of the proliferative response required the presence of the drug at both early and late stages of cell activation. Inhibition of mononuclear cell activation by cyclosporine A was not affected by isoprinosine. These results suggest that enhancement of mononuclear cell proliferation by isoprinosine involves events in both early and late stages of the activation cycle.

Antibodies, Monoclonal↗
PubMed1988

Defective dendritic cell accessory function in NZB/W F1 hybrid mice.

The proliferative response of NZB/W F1 hybrid mice when activated by sodium periodate (NaIO4) was found to be markedly defective as compared to the response in control NZW mice. This defect was observed in both 4 month old female mice and in 8-10 month old male mice. To determine whether the defect was an intrinsic T cell defect or an accessory cell defect, splenic dendritic cells (DC) were purified and their ability to activate enriched T cells after NaIO4 stimulation was assessed. In mixing experiments it was observed that normal NZW dendritic cells could restore the response of NZB/W F1 hybrid T cells whereas addition of NZB/W F1 dendritic cells to NZW T cells resulted in defective 3H-thymidine incorporation after NaIO4 stimulation. These results indicate that accessory DC of NZB/W F1 mice are defective and unable to support T cell responses to the mitogen NaIO4.

Animals↗
PubMed1987

Depressed 3H-thymidine incorporation by measles infected mononuclear cells can be corrected by treatment with isoprinosine or 5-fluoro-2-deoxyuridine.

Incorporation of thymidine by measles infected PHA-activated lymphocytes was found to be depressed although production of interleukin 2 (IL-2) and expression of IL-2 receptors on these cells was similar to that of non-infected cells. The decrease in incorporation of 3H-thymidine by infected cells was not due to cell death and could be restored by treating the cells with isoprinosine or 5-fluoro-2-deoxyuridine. These results suggest that the depressed incorporation of 3H-thymidine by measles-infected cells is not due to inhibition of early events required for lymphocyte proliferation, but is rather due to interference in the thymidine pathway required for the synthesis of DNA.

Antigens, Surface↗
PubMed1979

Desensitization of patients with bee sting allergy using pure bee venom.

Forty patients who had previously experienced severe systemic reactions after a bee sting were desensitized using pure bee venom. A modified 'Rush' regimen was employed whereby patients received two injections a week and reached maximal desensitization in 5 weeks. Eleven patients have subsequently been stung again and have developed no generalized reaction. Although this form of desensitization is considered to be highly effective in protecting sensitive patients, both generalized and local side-effects were frequent. Maintenance desensitizing injections are required every month for an indefinite period. It is concluded that desensitization with pure been venom should be undertaken only in highly selected sensitive patients, and should be performed under strict control.

Adolescent↗
PubMed1978

The effect of levamisole on E-rosette formation by trypsinized lymphocytes.

Normal lymphocytes treated with trypsin lost their ability to form normal numbers of rosettes with sheep red blood cells. The recovery in E-rosette forming capacity of trypsinized cells was considerably augmented when the cells were incubated in the presence of a wide range of concentrations of the immunostimulatory drug, levamisole. Substantial recovery of rosette-forming ability was seen 2 hr after incubation of trypsinized cells with levamisole.

Humans↗
PubMed1978

Inhibitory effect of prostaglandin A1 on neutrophil motility.

Using Boyden chambers, Prostaglandin A1 (PGA1) was shown to inhibit directed movement of polymorphonuclear (PMN) leucocytes to the chemoattractants endotoxin-activated serum and casein, and in random migration systems. Depressed chemotaxis could not be entirely attributed to defective random migration, as the drug was shown to inhibit both chemokinesis (stimulated random migration) and "true chemotaxis". In addition, PGA1 inhibited the movement of neutrophils out of capillary tubes and substantially reduced hexose monophosphate shunt (HMPS) activity. Mice injected with PGA1 demonstrated significantly less PMN movement into trypticase-soy-broth-induced peritoneal exudates, and it is postulated that during inflammatory processes release of PGA1 increases cell accumulation at the site, thereby amplifying the inflammatory response.

Chemotaxis, Leukocyte↗
PubMed1977

The effect of PHA-activated MN-cell supernatants on polymorphonuclear leucocyte function.

The effect of PHA-activated mononuclear-cell (MN) supernatants on various polymorphonuclear-leucocyte (PMN) functions were assessed. Treatment of PMN with PHA-activated MN-cell supernatants resulted in greater electrophoretic mobility, indicating an increase in the negative surface charge. PMN directional motility was inhibited in the presence of active supernatants but was not affected by a pulse exposure of the PMN to these supernatants. Neither control nor active supernatants were chemotactic for PMN, but treatment of these cells with active supernatants produced an increase in their phagocytic activity, their ability to reduce NBT and in their glucose oxidation through the hexosemonophosphate shunt. Bactericidal capacity of these PMN was unaltered. Specific loss of leucocyte inhibitory factor (LIF) activity from supernatants of PHA-activated MN cells followed their absorption with PMN cells but not with human MN cells or guinea-pig peritoneal exudate cells. Furthermore, acquired inhibition of migration of the absorbing PMN was observed.

Blood Bactericidal Activity↗
PubMed1976

Defective leucocyte inhibitory factor (LIF) production by lymphocytes in children with kwashiorkor.

Production of the lymphokine leucocyte inhibitory factor (LIF) by phytohaemagglutinin (PHA)-stimulated lymphocytes was assessed in 25 children with kwashiorkor. Although the lymphocytes of 12 of these patients produced adequate amounts of LIF, the rest of the group failed to produce lymphokine after PHA activation. There was no correlation between the ability to produce LIF and the age, severity of malnutrition or any other clinical parameters assessed in these patients. This finding confirms the presence of defective cell-mediated immunity observed in a substantial proportion of kwashiorkor children.

Humans↗
PubMed1976

Production of leucocyte migration inhibitory factor by neonatal lymphocytes.

Lymphocytes (mononuclear cells) from cord blood of 10 normal placentas and from 10 normal adults were assessed for production of leucocyte migration inhibiting factor (LIF) after phytohaemagglutinin (PHA) stimulation, as a measure of cell-mediated immunity. Mononuclear cells from both adult and cord blood produced adequate quantities of LIF, indicating that neonatal lymphocytes have the ability to manufacture normal amounts of lymphokines.

Adult↗
PubMed1976

The effects of cyclic AMP on leucocyte inhibitory factor (LIF) production and on the inhibition of leucocyte migration.

The effect of drugs known to increase intracellular levels of cyllic AMP were studied in the leucocyte migration ihibition system. It was found that cyclic AMP, dibutyryl cyclic AMP, theophyline, and prostaglandins E1 and E2 inhibited the production of leucocyte inhibiting factor by HA pulsed lymphocytes Inhibition only occured when the drugs were present during or after the PHA pulse. In addition it was found that these drugs enhanced the migration of polymorphonuclear leucocytes (PMN), in this system. Electrophoretic mobility of PMN cells was not altered by these drug indicating that the effect is not due to changes in membrane charge. However, granulocyte adhesion was reduced in the presence of these drug suggesting that adhesion is of primary importance in the migration of polymorphonuclear leucocytes out of capillary tubes. The findings show that cyclic AMP is important in modulating both cell-mediated and inflammatory responses.

Bucladesine↗
PubMed1976

Leucocyte capillary migration: an adherence dependent phenomenon.

To determine the mode of action of leucocyte inhibitory factor (LIF) on polymorphonuclear leucocyte (PMN) migration out of capillary tubes, this phenomenon has been compared with PMN adhesion to cotton wool columns. Colchicine and vinblastine sulphate had no effect on either of these processes but cytochalasin B caused marked inhibition of PMN migration and increased PMN adhesion. The cytochalasin B effect could be reversed in the presence of drugs known to increase intracellular levels of cyclic AMP. For inhibition of PMN migration by LIF, Mg2+ but not Ca2+ was essential. LIF not only inhibited PMN migration but also increased PMN adhesion to cotton wool columns. LIF inhibitory activity on PMN migration was not affected by colchicine or vinblastine. Leucocyte migration and adhesion depend on similar mechanisms, and are both influenced by LIF which probably acts by affecting micro-filament function.

Calcium↗
PubMed1976

In vitro reversal of cellular unresponsiveness induced by levamisole.

Mononuclear cells from twenty-one patients with depressed cellular reactivity were assessed for the ability to produce leucocyte inhibitory factor (LIF) and to transform after PHA stimulation, in the presence or absence of levamisole. Cells from nineteen patients failed to produce significant lymphokines when stimulated with PHA alone, but after a prior 1-hr levamisole pulse normal amounts of LIF were produced. Unstimulated mononuclear cell supernatants from six patients showed LIF-like activity, which could be abolished or decreased in five of the six when the cells were initially treated with levamisole. Mononuclear cells from seven of twelve patients which failed to incorporate [3H]thymidine after PHA activation, showed an increased response after a 1-hr levamisole pulse. Unstimulated mononuclear supernatants from six patients inhibited the lymphoproliferative response of normal cells to PHA. After treatment with levamisole, however, the suppressive effect of these supernatants was decreased or abolished. In vitro levamisole treatment, therefore, not only restores cellular responsiveness in anergic patients but also restricts the uncontrolled release of inhibitory factors.

Cells, Cultured↗