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Biomedical subjects

J Clot

Publications and source records attributed to J Clot.

At least 109 records · Page 6Linked to original sources

Circulating lymphocyte subpopulations in juvenile insulin-dependent diabetes. Correction of abnormalities by adequate blood glucose control.

Circulating lymphocytes from 39 juvenile insulin dependent diabetics of recent onset were studied by six membrane marker techniques and mitogen stimulation. Well controlled (n = 14) were grouped separately from poorly controlled (n = 25) patients. The total lymphocyte counts were not different from 50 control subjects. The percentage of T-cells detected by erythrocyte rosettes and B-cells detected by erythrocytes--antibody--complement rosettes was significantly decreased only in poorly-controlled diabetics (64.1 +/- 1.3 and 9.7 +/- 1.8, vs 71.0 +/- 1.0 and 15.3 +/- 0.6 in controls). Cells bearing receptors for the Fc fragment of IgG immunoglobulins were decreased in both groups. Mitogen stimulation was not different from controls but was significantly lower in poorly controlled than in well controlled diabetics. Optimal blood glucose control for 5 +/- 2 days using an external artificial pancreas led to a rapid normalisation of membrane marker values and mitogen responsiveness of lymphocytes from previously poorly controlled diabetics. Separate in vitro experiments showed that glucose had an inhibitory effect on mitogen stimulation at concentrations greater than or equal to 8.3 mmol/l and on T- and B-lymphocyte numbers at concentrations greater than or equal to 55.6 mmol/l. DL 3-hydroxybutyrate tested at 17.1 and 34.2 mmol/l only depressed mitogen responsiveness. Such results suggest a rapidly reversible T-cell defect closely linked to the existing metabolic disturbances.

Adolescent↗

T-, B- and Fc-gamma-receptor-bearing lymphocytes in asthma.

T-, B- and Fc-gamma-receptor-bearing lymphocytes were detected using six different membrane markers in patients suffering from asthma having either normal or low serum IgA levels. E rosettes, aE rosettes and a human anti-T lymphocyte antiserum (HTLA) were used for T cell determination. In patients with low serum IgA levels E rosettes were significantly decreased. B lymphocytes were identified by EAC rosette formation and visualization of surface membrane immunoglobulins (SmIg). No significant difference was seen. Fc-gamma-receptor-bearing lymphocytes were assessed by the EA rosette assay and were significantly decreased in asthmatics with normal IgA levels. This result might be explained by the presence of immune complexes.

Adolescent↗

[Suppressor cells of mitogen responses during rheumatoid polyarthritis].

The suppressor activity of mononuclear cells of the peripheral blood (MCPB) during rheumatoid polyarthritis (RP) was studied using experimental protocole. The MCPB stimulated in vitro by concanavaline A (Con A) are capable of suppressing the mitogenis response of autologus cells; moreover, the short-lived spontaneous suppressor cells disappear during 24 hour in vitro incubation that determines an increase in the proliferative response of the incubated cells for 24 hours. In two of the six RP studied, the suppressor activity generated Con A and the spontaneous suppressor activity are nul. Culture experiments with the MCPB of PR and control subjects show that this defect in suppressor activity is more related to a problem in the generation of suppressor cells than to a deficiency in the response to suppressor signals.

Arthritis, Rheumatoid↗

Lymphocyte markers, serum thymic factor and IgE in IgA deficiency.

Eleven patients having a selective IgA deficiency had very low T-cell percentages assessed by using E-rosettes, active E-rosetts and an anti-human anti-T-lymphocyte antigen serum. B-cells were normal or slightly decreased. IgE concentrations were often low. Patients with serum IgA under 50 IU/ml often had elevated serum IgE values and low T-cell percentages. Serum thymic factor dosages were correlated with the E-rosette assay.

Adolescent↗

[Pathogenesis of psoriasis].

Psoriasis is basically an excessive proliferation of the epiderm. This state results mainly from an imbalance in the cyclical nucleotides linked mainly to anomalies of the keratinocyte membranes. The membrane change is due to antibodies whose production may be dependent upon a deficit of a T-lymphocyte sub-population. This deficit may be considered the result of the penetration of virus agent with the help of multiple genetic factors. The various link of this pathogenic chain may be modified by numerous external factors which, by causing a worsening in a pre-existing imbalance, brings about the appearance of lesions.

Antibody Formation↗

[Physiopathology of rheumatoid psoriasis].

The physiopathology of rhumatoid psoriasis (RP) is poorly known. Besides the genetic factors we study immunological disorders from a series of 51 cases. We found mainly an increase of serum IgA, a decrease of IgM, a low level of circulating immune complexes, sometimes IgG type antiglobulin factor (very seldom IgM type, which explains the sero-negativity) seldom antinuclear antibodies; we found also a diminution of T lymphocytes detected by a decrease of E rosette - forming cells and an increase of the lymphocyte subpopulation forming high avidity EA rosettes, whereas the mitogenic response is normal or slightly decreased in the presence of Con A (not significant). A increased frequency of HLA DRW5 and DRW2 was found but too few cases were studied to make possible a definite conclusion. This immunopathologic profile is compared to that of psoriasis with anthropathy. The relevance of immune disorders in the physiopathology of RP is discussed.

Adolescent↗

[B-immunoblast lymphosarcoma 8 years after a malignant reticulosis].

A girl presented with a malignant reticulosis in the early months of life. For 4 years she was treated with repeated courses of irradiation and chemotherapy, mostly cyclophosphamide. After 6 years of complete remission she developed a rapidly progressive B cell lymphoma. The contribution of the various forms of treatment to the development of the second malignancy are discussed.

Bone Neoplasms↗

[The pathogenesis of psoriasis : realities and hypotheses (author's transl)].

Our pathogenic pattern, may be summarised in 7 propositions : - psoriasis is a proliferative disease of the epidermis. - the increased mitotic activity is related to imbalance of cyclic nucleotides and of prostaglandins. - this imbalance may be explained by abnormalities of the membranes of the keratinocytes. - this alteration in cell membranes results from immunological phenomena located in psoriatic epidermis. - the disturbance of immunity with production of auto-antibodies may be related to a deficiency in a sub-population of thymus-dependent lymphocytes. - this cyclic deficiency could be due to a viral agent whose penetration and persistence in the body would be dependent upon multiple genetic factors. - numerous external factors may act upon the various steps of this pathogenic chain, to worsen a pre-existent imbalance and precipitate the development of the lesions.

Antibodies, Antinuclear↗

[Sézary's syndrome (author's transl)].

The syndrome described in 1938 by Sézary and Bouvrain is characterized by a possibly hyperpigmented erythroderma with oedema and infiltration of the skin, palmo-plantar keratoderma, diffuse alopecia and large lymphadenopathies. The cutaneous histopathology frequently shows a dermal mononuclear infiltrate with, sometimes, epidermal microabcesses. But none of these signs is actually specific for the Sézary syndrom, the only criteria of which is the presence of circulating Sézary cells with their folded, cerebriform nucleus demonstrated by electron microscopy. The Sezary cell is to date clearly identified as a T lymphocyte but membrane markers and Tcell fonction studies could elicite abnormal and poor reactive T cell. In order to assert the Sézary Syndrome it is stated by the authors that the erythroderma must be associated with more than 10% of Sézary cells in peripheral blood. This feature is needed to differentiate the Sézary syndrome from the erythrodermic form of mycosis fondoïdes in which the abnormal T cell proliferation is mainly located in the skin. The relationship with the T cell chronic lymphatic leukemia and the main treatments of the Sezary syndrome are discussed.

Dermatitis, Exfoliative↗

Immunologic aspects of psoriasis. III. Fc-gamma-receptor bearing mononuclear cells in peripheral blood.

An anti-IgG activity has previously been reported at the cellular level in patients with psoriasis. This activity was demonstrated by the so-called 'rheumatoid' rosette test. In the present work the nature of 'rheumatoid' rosette-forming cells was studied in comparison with other EA rosette techniques. The use of purified cell populations showed that the lymphocytes participating in the 'rheumatoid' rosette phenomenon were lacking conventional T and B cell membrane markers, and were thus referred to as null cells. Such mononuclear cells bearing a receptor for the Fc part of IgG were able to act as killer cells to IgG-coated target cells. The cytotoxic activity was mainly restricted to a small proportion of lymphocytes forming 'rheumatoid' rosettes which had a high avidity for EA complexes. Such cytotoxicity could contribute to the aetiology of lesions in psoriasis.

Antibody-Dependent Cell Cytotoxicity↗

Age-dependent changes of human blood lymphocyte subpopulations.

T- and B-lymphocyte populations were enumerated at four stages of life: at the newly born, infant, adult and aged stages. The proportion of T cells detected by E rosettes and an anti-human T-lymphocyte antigen (HTLA) serum incresed from new-born children to adults, then decreased with ageing. The antiserum detected less mature T cells in aged people. The percentages of cell forming 'active' E rosettes increased with ageing. Lower numbers of B cells bearing surface immunoglobulins were found in adults.Complement receptor-bearing lymphocytes (percentages and absolute numbers) decreased from new-born children to aged humans. Finally, the number of monocytes were significantly greater in the young than in adult and aged people. Such results bring new data concerning the age-dependent changes of lymphocyte subpopulations and concerning the significance of various techniques used together to detect mononuclear cell populations in the human peripheral blood.

Adult↗

[In vitro study of cellular immunity in atopic and in contact eczema (author's transl)].

Peripheral blood lymphocytes from 20 atopic dermatitis patients, 10 contact dermatitis and 50 healthy subjects were studied by the following methods: E rosettes, active E rosettes anti-HTLA serum (T cells), surface immunoglobulins (B cells), Ea rosettes (Fc-gamma-receptor bearing cells) stimulation by PHA, ConA, PWM. In contact dermatitis the results only indicated significantly low percentages of active E rosettes (whereas E rosette, HTLA, surface immunoglobulins, Ea rosettes are normal) and a poor response to PHA and ConA. In atopic dermatitis the presence of a T cell defect was assessed by low percentages of E rosettes. However normal results obtained with an anti-HTLA serum indicated that this T cell defect was not quantitative but could be due to intrinsic lymphocyte abnormalities or serum factors. Moreover the percentage of B cells was significantly increased. The stimulation index was lower after ConA than after PHA stimulation. This could be in favor of a T suppressor cell impairment. The place of this T cell defect in atopic dermatitis and the possible correlations with the Sczentivanyi's theory are discussed.

Adolescent↗

[Fc-gamma-receptor cells and rheumatoid arthritis].

Certain blood lymphocytes of patients suffering from rhumatoid arthritis (RA) and or control subjects, can be detected using a rosette technique in the presence of erythrocyte antibody compounds (EA). The EA rosettes demonstrate the presence of cells having a receptor for the Fc fragment of the IgG's (Fc-receptor). A significant increase in highly active EA rosettes during RA was demonstrated using six EA compounds differing according to the type of erythrocyte and the quantity of sensitizing antibody. These highly active EA rosettes correspond to the case in which few antiserum molecules cover the erythrocytes. Their high level in RA may correspond to an increased number of Fc-receptor cells or to a stronger linkage of EA compounds. The cells forming EA rosettes are responsible for the resulting cell antibody cytotoxicity that seems to change little during rhumatoid disease. However, the very special behavior of Fc-receptor lymphocytes incubated in vitro suggests that the IgG receptors are modulated by the immune compounds present during RA.

Adult↗