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P Segond

Publications and source records attributed to P Segond.

At least 37 records · Page 2Linked to original sources
PubMed1982

Impaired primary in-vitro antibody response in progressive systemic sclerosis patients: rôle of suppressor monocytes.

The primary in-vitro antibody response developed by peripheral blood mononuclear cells (PBM) towards trinitrophenyl coupled to polyacrylamide beads (TNP-PAA) was evaluated in 17 untreated patients with progressive systemic sclerosis (PSS). This response was markedly depressed as compared with that of 19 control patients and 28 normal subjects. In eight PSS patients and eight normal controls the anti-TNP response was measured before, and after, a PBM filtration on nylon wool columns. This procedure dramatically reduced the proportion of monocytes identified as mononuclear cells staining positively for peroxidases, and restored the response of PSS PBM to the level observed in normal PBM. In four experiments, plastic-adherent cells from either normal subjects of PSS patients were added to autologous nylon-passed PBM. This did not modify the response from normal PBM but inhibited the response of PSS PBM. The inhibitory effect of PSS plastic-adherent cells was insensitive to a 2,000 R X-ray irradiation. These results strongly suggest that the impaired in-vitro antibody response observed in PSS can be attributed to a suppressor monocyte. The concanavalin-A-induced suppressor cells of the antibody response were assayed in PSS. They exerted a suppressive effect to the same extent as in controls.

Adolescent↗
PubMed1980

Depressed primary in vitro antibody response in untreated systemic lupus erythematosus. T helper cell defect and lack of defective suppressor cell function.

The in vitro antibody response of peripheral blood lymphocytes (PBL) from 19 patients with untreated systemic lupus erythematosus (SLE) was compared with that of 20 control patients and 44 normal subjects. Trinitrophenyl polyacrylamide beads (TNP-PAA) were used to induce IgM anti-TNP plaque-forming cells. SLE patients displayed a markedly depressed, and in most instances virtually absent, response. This was not due to an unusual kinetics of the response; nor could it be induced by preincubation of SLE patients' PBL. In co-cultures of SLE patients and normal PBL, the former, with few exceptions, did not exert a suppressive effect. In four patients the anti-TNP response of either unfractionated or T-depleted SLE PBL could be restored by T cells from a normal individual. Conversely in three of these patients, SLE T cells could not support the response of normal B cells, suggesting a T helper cell defect in SLE PBL. Concanavalin A (Con A)-induced suppressor cells of the antibody response could be assayed by two approaches: (a) in responder SLE patients, by the direct addition of Con A to TNP-PAA-stimulated cultures; (b) in seven patients by transfer of Con A-activated cells to the responding culture of a normal allogeneic donor. In both cases SLE PBL were able to exert a suppressive effect to the same extent as normal PBL.

Adult↗
PubMed1979

[Exploration of humoral immunity in man using blood lymphocytes cultures (author's transl)].

New methods allow the study of humoral immunity in man using blood lymphocyte cultures. A primary in vitro antibody response can be induced, characterized by the appearance of antibody forming cells, and its pattern is as follows: stringent culture requirements, which have been so far obtained in few laboratories; the kinetics of the response, with a peak on day 7--8; and exclusively IgM response; a T-cell requirement. Among these methods, the model we have described has the advantage of allowing a reproductible response in a given individual. The in vitro study of humoral immunity has limitations, the most apparent of which is that it addresses itself to only one lymphoid population, that in peripheral blood, easily accessible. It presents several advantages, as compared to an in vivo study after injection of an antigen: absence of ethical problem; the necessity of only one blood sample, at a given time, avoiding the interference of a treatment started after the test; the possibility of performing successive primary stimulations for a longitudinal study.

Acrylamides↗
PubMed1979

Depressed primary in vitro antibody response in rheumatoid arthritis.

We have studied the primary in vitro antibody response toward a hapten in cultures of peripheral blood lymphocytes from twenty-two patients suffering from regular rheumatoid arthritis (RA). These patients were not receiving immunosuppressive drugs or corticosteroids and had not taken Aspirin or non-steroidal anti-inflammatory agents for at least 72 hr. The control groups included thirty-two healthy subjects and twenty-seven control patients. The mean anti-TNP response of the RA patients was significantly lower than that of both control groups. No pre-existing anti-TNP or IgG response could be detected. A search for suppressor cells in co-cultures of RA and normal lymphocytes was negative. On the contrary, the extent of allogeneic enhancement in such co-cultures was comparable to that observed when control lymphocytes were co-cultured. RA serum added to normal lymphocytes cultures showed a dramatic inhibitory effect in only two out of nine cases. A follow-up study has strongly suggested that RA lymphocytes could increase their in vitro antibody response upon treatment.

Adult↗
PubMed1979

[In vitro study of the primary antibody response of circulating lymphocytes in patients with chronic inflammatory rheumatism].

We have studied the in vitro antibody response to a hapten of peripheral blood lymphocytes from 26 patients with rheumatoid arthritis and 7 ankylosing spondylitis. These patients had never received immunosuppressor drugs before or corticosteroids during the month before the test. They had failed to receive aspirin or non-steroid anti-inflammatory drugs for 72 hours before blood sampling. The control groups included respectively 38 healthy subjects and 24 patients hospitalized for non inflammatory disease. The antibody response of ankylosing spondylitis patients is comparable to that of controls ; on the opposite the response of patients with rhumatoid arthritis is significantly depressed in comparison with the three other groups. The weak response of lymphocytes in arthritis is not due to increased cell death in culture or to modified kinetics of the antibody response or to the appearance of a IgG secondary type response or a in vivo pre-activation. The lymphocytes of arthritis patients do not inhibit the response of normal lymphocytes when they are co-cultured. The observed response is identical to that obtained when control patient lymphocytes are co-cultured with normal lymphocytes. The function of suppressor T cells induced by Con A seems normal in spondylitis and arthritis.

Adult↗
PubMed1979

Regulation of the primary in vitro antibody response in human peripheral blood lymphocytes: different effects of mitogen-induced and spontaneous T suppressor cells.

The specific response of human peripheral blood lymphocyte cultures to TNP-polyacrylamide was suppressed by the addition of concanavalin A (Con A). A dose of Con A (0.5 microgram/ml) could be selected, which induced a reproducible but incomplete suppression independent of the magnitude of the anti-TNP response. Con A-stimulated cells could transfer the suppression to autologous or allogeneic responding cells. The suppressor activity was present in the E-rosette forming cell fraction and was abolished by mitomycin C treatment prior to incubation. With a particular batch of foetal bovine serum, spontaneous suppressor cells were produced which suppressed the response of autologous and allogeneic lymphocytes. In allogenic mixtures, the otherwise enhancing allogeneic effect was replaced by a marked suppression from spontaneous suppressor cells. This suppression was higher than that exerted on autologous lymphocytes, suggesting that an unexpected negative allogenic effect had taken place. Spontaneous suppressors were ineffective when added on day 2 of a culture responding to TNP-polyacrylamide, whereas Con A induced suppressors were fully effective.

Acrylamides↗
PubMed1979

[Cryoglobulins and circulating immune complexes in rheumatoid arthritis. Clinical and biological correlations].

We studied circulating immune complexes using a test involving the precipitation of these complexes with polyethylene glycol 6000 at 2.5 percent, and characterization of the Clq bound in vivo to immunoglobulins in the serum of 126 healthy subjects, 95 hospitalized controls and 181 patients suffering from rheumatoid arthritis (RP). Likewise, the RP benefited from a study of cryoglobulins (CG). The PEG-Clq proved positive (PEG +) in 7 per cent of the healthy controls, 25 per cent in the seronegative RP. ThePEG & RP have a level of proteins, gammaglobulins, IgM and IgG that is higher than in patients in whom the test is negative. On the other hand, they have a lower level of C4. One CG was detected in 43 patients who were all PEG +. The level of CG is proportionate to the intensity of the articular inflammation, the sedimentation rate, the level of seric iron and that of hemoglobin. The composition of the precipitins obtained by activity of the PEG is very close to that of the CG.

Adolescent↗
PubMed1976

[IgM myeloma].

The authors report the case of a 62 year old woman in whom bony pain led to the discovery of lacunar osteolytic appearances, in particular in the skull, abnormal medullary plasmacytosis and serum monoclonal immunoglobulin with Bence-Jones proteinuria. The case was unusual as the immunoglobulin observed was an IgM. This finding led the authors to a critical revision of the distinctive characteristics of multiple myeloma and Waldenström's macro-globulinemia, emphasizing the distinguishing value of the cytological criterion. The authors recall the various neoplastic proliferations of the B lymphocytes at the various stages of their maturation and emphasize the predominance of monoclonal IgM during proliferations affecting the early stages of maturation of the B lymphocytes and the rareness of these IgM during plasma cell neoplasms.

B-Lymphocytes↗