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Biomedical subjects

J F Delfraissy

Publications and source records attributed to J F Delfraissy.

At least 145 records · Page 8Linked to original sources
PubMed1986

[Transient remission after viral infection in 3 patients with chronic autoimmune thrombopenia].

We describe three patients with chronic autoimmune thrombocytopenia who exhibited transient remission during viral infection (varicella, hepatitis B, and influenza virus pneumopathy). In two patients, a male homosexual and an hemophiliac, thrombocytopenia was associated with AIDS-related complex. The third patient had classic idiopathic thrombocytopenic purpura. The mechanism of these rare remissions is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Suppressor T cell induction by soluble OKT3 antibody does not require cross-linking of the T3 molecule.

The monoclonal antibody OKT3 can induce T suppressor cells of the in vitro antibody response when used at concentrations as low as 10 ng/ml and in cultures containing as few as 4% OKT3-pretreated T cells. These suppressor cells are radioresistant, cyclosporin sensitive and belong to the T4 as well as the T8 subpopulations. In contrast with the mitogenic effect of OKT3 the suppressor activity can be induced and expressed in highly monocyte-depleted cultures. Moreover F(ab')2 fragments of OKT3, although not mitogenic, are able to induce suppressor cells. Thus cross-linking of the T3 molecule (such as that realized when intact OKT3 IgG and monocytes are present) is not required to induce suppressor cells among resting normal T cells.

Antibodies, Monoclonal↗
PubMed1985

[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↗
PubMed1985

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↗
PubMed1985

[Simultaneous detection of IgM antibodies against the hepatitis A virus and the viral capsid antigen of Epstein-Barr virus in acute hepatitis].

The simultaneous detection of IgM antibodies to hepatitis A virus (anti-HAV IgM) and IgM antibodies to viral capsid antigen (anti-VCA IgM) of Epstein-Barr virus (EBV) in patients with acute viral hepatitis has led us to systematically study serological markers of EBV in patients with anti-HAV IgM positive acute hepatitis and to test for anti-HAV IgM in sera of patients with acute hepatitis associated with serological evidence of current primary EBV infection. All patients studied were HBsAg negative and were not drug-addicts, nor homosexuals. In 15 consecutive patients with anti-HAV IgM positive acute hepatitis, anti-HAV IgM and anti-VCA EBV IgM antibodies were simultaneously detected in 9 cases. Of these 9 patients, antibodies to nuclear antigen were positive in 8 cases, antibodies to early antigen were positive in 7 cases and rheumatoid factor was positive in 4 cases. In 5 consecutive patients with acute hepatitis associated with serological evidence of current primary EBV infection, anti-HAV IgM was not detected. Simultaneous presence of anti-VCA EBV IgM, early antigen IgG antibodies and nuclear antigen antibodies in 7 patients with acute hepatitis associated with anti-HAV IgM suggests reactivation of EBV or reactivation of clones secreting antibodies anti-EBV in HAV infections. Furthermore, these results show that anti-VCA IgM only cannot be considered to be a specific marker of early EBV infection in patients with acute hepatitis.

Acute Disease↗
PubMed1985

Functional properties of two human B cell growth factor species separated by lectin affinity column.

The supernatants from PHA-activated normal human T cells (conditioned medium) were fractionated by differential adsorption on Con A-Sepharose columns. The effluent contained both IL 2 activity (tested on the CTL-L2 cell line) and BCGF activity (tested on anti-mu-activated normal B-enriched cells). Absorption of such effluent on PHA-activated T cell blasts removed the IL 2 activity without affecting the BCGF activity. The eluate also displayed BCGF activity (tested on anti-mu-activated B-enriched cells) without detectable IL 2 activity. The two BCGF species isolated by this criteria synergize with semipurified IL 1 to support the anti-mu-induced proliferation of highly monocyte-depleted B cells. Both BCGF species required the presence of anti-mu Ab to support the proliferation of small B cells (at the G0 stage). However, in contrast to crude conditioned medium and to the BCGF present in the effluent, the BCGF present in the eluate was unable to induce the proliferation of unfractionated or large (at the G1 stage) B cells in the absence of anti-mu Ab. These results support the existence of two functionally different human BCGF species, differing at least in their relative sugar content and distinct from IL 2.

Adsorption↗
PubMed1984

[Eosinophilic cystitis of allergic origin].

Eosinophilic cystitis, of which 35 cases have been published, is a recurrent cystitis remarkable for its chronicity and for the importance of haematuria; the urine is usually sterile and blood eosinophilia frequently present; at histology, infiltration of the vesical wall by eosinophils is pathognomonic. In view of the irregular results of cortico-steroid treatment, a search for causative factors is required. Parasitic infestation has been suspected but never actually proven, and an allergic origin probably is frequently missed. We report two cases of eosinophilic cystitis where allergy to penicillin and clometacin respectively could be demonstrated for the first time and in which the condition subsided after withdrawal of these drugs.

Analgesics↗
PubMed1984

Helper T cell activation for the human B cell response to trinitrophenylated polyacrylamide beads: involvement of the T4 antigen.

The monoclonal antibody (mAb) OKT4A (but not OKT4) inhibits the in vitro antibody response of human peripheral blood mononuclear cells. The target of OKT4A mAb is the helper T cell, as the helper cells for the antibody response to trinitrophenylated polyacrylamide beads (TNP-PAA) are exclusively in the T4 subset. The OKT4A mAb is still suppressive when the anti-TNP response of cultures of monocyte-depleted cells is supported by purified interleukin 1. Both the OKT4A mAb and anti-DR mAb suppress the non-specific T cell proliferation in the cultures leading to the in vitro mAb response. A parallel inhibition is observed for the autologous mixed lymphocyte reaction, the nonspecific B cell response, but the T cell response to mitogens is not affected. These results suggest that the recognition of self major histocompatibility complex class II determinants by the T4 molecule plays a major role in the activation of T helper cells for antibody production to this particulate antigen.

Acrylic Resins↗
PubMed1984

Interleukin 1 can replace monocytes for the specific human B-cell response to a particulate antigen.

It is shown that the anti-trinitrophenyl (TNP) response of human B cells to trinitrophenyl polyacrylamide beads (TNP-PAA) is monocyte dependent. This response is abolished by extensive adherent cell depletion and restored by the addition of monocytes. The optimal response is obtained with 3% monocytes, higher numbers being suppressive. Supernatants from muramyl dipeptide (MDP)-activated monocytes can restore the response of monocyte-depleted preparations even when cells are cultured at suboptimal concentration. A partially purified preparation of interleukin (IL-1) has a comparable restorative ability. The following arguments suggest that monocytes do not function as antigen-presenting cells for this particulate antigen: (i) antigen-pulsed monocytes induce neither an anti-TNP response nor a specific T-cell proliferative response; (ii) allogeneic monocytes function as well as autologous monocytes to restore the response of nonadherent cells; (iii) HLA-DR-negative cells from the human leukemia cell line K562 can replace monocytes for this response. Monocyte supernatants do not replace T cells for the response of B-enriched lymphocytes, showing that T cells are directly involved in B-cell activation.

Acrylic Resins↗
PubMed1984

[Glomerular nephropathies in untreated rheumatoid arthritis. Review of the literature apropos of 2 cases].

Two cases of classical rheumatoid arthritis complicated by the development of a glomerulopathy independently of drug treatment are presented. Renal biopsy showed membranous glomerulonephritis in one case and fusion of foot processes in the second. The literature is reviewed and the possible relationships between rheumatoid arthritis and these glomerulopathies are discussed. The authors conclude to the absence of causal relationship between these two diseases.

Aged↗
PubMed1984

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↗
PubMed1983

[Acute renal insufficiency with ketoprofen and clometacin].

Several recent reports emphasize the adverse effects of non-steroidal antiinflammatory drugs on renal function. These reports incriminate several phenylpropionates but none involve ketoprofen. There have been no indications that clometacin has renal toxicity. We report a case of acute renal failure which occurred during therapy with both ketoprofen and clometacin. The onset of renal failure after their administration, the return to normal renal function once therapy was discontinued and the absence of any other detectable etiology make the responsibility of the treatment very likely. The different possible mechanisms and the role of underlying disease and of associated therapy are discussed. In the index case the reduced excretion of urinary prostaglandin E2 suggests inhibition of prostaglandin synthesis rather than direct drug toxicity or an immuno-allergic mechanism.

Acute Kidney Injury↗