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J Dormont

Publications and source records attributed to J Dormont.

At least 55 records · Page 3Linked to original sources

[Activation of human B lymphocytes by a particulate antigen].

A specific IgM antibody response toward the trinitrophenol (TNP) hapten can be induced in mononuclear blood cell suspensions upon culture with a particulate antigen: polyacrylamide beads conjugated with the TNP hapten (TNP-PAA). The response, and its specificity, are demonstrated by an increase in the number of TNP binding B lymphocytes (specific rosette forming cells), by the appearance of cells producing anti-TNP antibody at a high rate (haemolytic plaques), (ELISA test). The anti-TNP response requires monocytes, the role of which is to produce interleukin-1 (IL-1) and T lymphocytes (belonging to the T4 helper subset) the role of which is to produce interleukins (the characterization of which is under study). We propose a model or B cell activation based on the following signals: an early specific signal, provided by the particulate antigen; several non specific signals, provided by T derived interleukins. The anti-TNP response is negatively regulated by monocytes, the functional states of which can be modified in certain situations (autoimmunity, aging) or influenced by glucocorticoids. Suppressor T lymphocytes of this response (not exclusively of the T8 phenotype) can be induced and this can allow the evaluation of T suppressor cell function. This was used in adult idiopathic thrombocytopenic purpura treated with high doses of intra-venous gammaglobulins.

Acrylic Resins↗

Suppressor cell function after intravenous gammaglobulin treatment in adult chronic idiopathic thrombocytopenic purpura.

Intravenous gammaglobulin (IVIgG) was given to seven adults with chronic idiopathic thrombocytopenic purpura (ITP). In parallel with platelet count, we studied Con A induced suppressor cell function for the autologous in vitro B cell response, T cell subsets and PAIgG levels, immediately before and 3-4 d after completion of treatment. Before treatment all patients had normal T cell subsets, decreased T suppressor cell function and increased levels of PAIgG. After IVIgG infusions, two patients were unresponsive and neither suppressor cell function nor PAIgG levels varied. In contrast, in the five responding patients we found an improvement in suppressor cell function and a decrease in PAIgG levels, while T cell subsets remained unmodified. Such results were reproducible in three patients after a second series of gammaglobulin infusions. Our results support the hypothesis that IVIgG infusion, apart from its effects on the reticuloendothelial system, may modulate the immune response by enhancing suppressor T cell function.

Adult↗

Inhibition of in vitro immunosuppressive effects of glucocorticosteroids by a competitive antagonist RU-486.

The 19-nor-steroid RU-486 is an antagonist of glucocorticosteroids acting competitively at the receptor level. Pharmacological and endocrinological studies have already shown that RU-486 is able to reverse glucocorticosteroid effects. The present study shows that RU-486 can counteract the inhibitory effect of glucocorticosteroids in two highly corticoid-sensitive in vitro immune responses: murine in vitro antibody response and human autologous mixed lymphocyte reaction.

Animals↗

Captopril and immune regulation.

We examined the in vitro effect of captopril (2.5 to 5 micrograms/ml) on the primary antibody response of human B cells. Captopril suppresses (by 50%) the specific anti-trinitrophenyl (TNP) response of unfractionated peripheral blood mononuclear cells (PBM) but not that of nonadherent PBM. The susceptibility to captopril suppression can be restored in the latter cell cultures by 10% adherent radioresistant cells. This suppression is independent of prostaglandins. In transfer experiments, cells preincubated with 5 micrograms/ml captopril suppress the antibody response of autologous nonadherent PBM. The inductive phase of this suppression requires both adherent cells and radiosensitive T cells. Once induced, the suppression can be transferred by isolated T effector cells. In vivo after a unique oral intake of captopril a moderate suppressor activity can be demonstrated in adherent cells from normal individuals. We conclude that captopril interferes with the immune regulation by inducing a suppressor circuit involving monocytes and a T8 suppressor effector lymphocyte.

Antibody Formation↗

[Acute kidney failure: age is not a factor in the prognosis].

The mortality of acute renal failure (ARF) remains distressingly high despite intensive dialysis and remarkable advances in critical care medicine. This lack of survival improvement may be due to an increased frequency of septic ARF and/or the association with multiple organ dysfunction. The role of age, as a factor indicative of a poor prognosis is a matter of controversy. To evaluate this role we have analysed the final outcome of 103 patients with ARF treated between october 1978 and february 1982 by one or more hemodialysis. The average age was 65.1 +/- 14.9 years (mean +/- standard deviation): 64 patients were over 65 years of age (74.7 +/- 10.2), 39 were under this age (47.5 +/- 14.4). Septic causes were found in 64 cases. Sixty eight patients (66%) died during the period of ARF. Mortality was 67% in patients under 65 years of age and 66% in patients over this age (p greater than 0.90). The outcome of septic ARF was independent of age (mortality rate: 79% for patients less than 65 years, 81% for patients greater than 65 years (p greater than 0.90)). The poor prognosis is probably related to multiple organ dysfunction and specially to acute respiratory distress (89% mortality). It can be concluded that patient's age does not worsen the prognosis of ARF.

Acute Kidney Injury↗

[Immunologic deficiency linked to aging. Role of monocytes].

The capacity of mononuclear cells from individuals over 70 years of age to mount a primary in vitro antibody response is profoundly decreased. We show that the removal of a nylon-adherent cell restores this response. The suppressor cell is plastic adherent, phagocytic non-T and radio-resistant, thus probably a monocyte. Its effect is inhibited by indomethacin, which suggests that its action if mediated by prostaglandins.

Adult↗

Immediate effects of captopril in acute left ventricular failure secondary to myocardial infarction.

In eight patients with acute left ventricular failure secondary to myocardial infarction the haemodynamic effects of captopril (25 mg), an orally active converting enzyme inhibitor, were measured. Haemodynamic modifications were maximal at 60 min and lasted for 2-3 h. Pulmonary wedge pressure fell from 23.5 +/- 4.9 (mean +/- SD) to 16.8 +/- 4.7 mmHg (P less than 0.01), cardiac output rose from 3.24 +/- 1 to 4.05 +/- 0.91 1/min (P less than 0.01). Systemic vascular resistance decreased from 27.34 +/- 3.81 to 17.52 +/- 1.65 mmHg min l-1 (P less than 0.01). Mean arterial pressure fell from 89.6 +/- 13.9 to 75.7 +/- 16.3 mmHg (P less than 0.001) while heart rate was not significantly modified. Six patients who had high pretreatment plasma renin activity values responded by a decrease in ventricular filling pressure and/or an increase in cardiac output. One patient with normal initial plasma renin activity value showed similar haemodynamic effects. THese data suggest that in the short term captopril is a vasodilator with both arterial and venous effects and improves cardiac function in acute left ventricular failure secondary to myocardial infarction.

Acute Disease↗

Specificity of antibodies to heterologous glomerular and tubular basement membranes in various strains of mice with different H-2 types.

C3H, CBA (H-2k) and NZB (H-2d) mice were immunized with dog insoluble glomerular (GBM) or tubular basement membrane (TBM). The titre of circulating antibodies was sequentially determined and their specificity was analysed using various soluble antigenic fractions. Glomerular and tubular deposits were studied on serial biopsies by direct immunofluorescence. After elution from whole kidneys, IgG fixation on normal mouse kidney sections was analysed by indirect immunofluorescence. After immunization with insoluble GBM, animals from all three strains develop antibodies mainly directed against collagenous antigenic determinants shared by GBM and TBM. After immunization with insoluble TBM, the antibodies are directed in NZB mice against non-collagenous TBM-specific determinants, in C3H mice against collagenous determinants and in CBA mice against both types of antigenic determinants. Thus the ability to respond to the various antigens of GBM and TBM is genetically determined and does not depend only on the major histocompatibility complex.

Animals↗

Primary in vitro antibody response in human cord blood lymphocytes.

Human cord blood lymphocytes were stimulated with trinitrophenyl--polyacrylamide beads (TNP--PAA) in order to induce a primary IgM anti-TNP response. With few exceptions, no anti-TPN response was obtained, whereas peripheral blood lymphomonocytic cells (PBL) from 18-mth-old children were able to respond to TNP-PAA. The addition of lipopolysaccharide (LPS) or of mitomycin-treated adult PBL to cultures of cord blood lymphocytes significantly enhanced their anti-TNP response, thus showing that functional anti-TNP B cell precursors are present in the human neonate.

Acrylic Resins↗