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Biomedical subjects

M Faure

Publications and source records attributed to M Faure.

At least 235 records · Page 13Linked to original sources

OKT8 human phenotype expressed by Papio papio monkey lymphocytes.

The potential cross-reactivity between human and Papio papio monkey lymphocyte antigens was investigated using various monoclonal antibodies specific for human T cell subsets and HLA-DR antigens. Monkey circulating lymphocytes expressed the OKT8 antigen, specific for the suppressor/cytotoxic T cell population and the HTLA antigens. These reactivities were also detected on lymphoid cells in the thymus and lymph nodes of the Papio monkey.

Animals↗

Pemphigus, pemphigoid, and epidermal upper-cytoplasmic antigens: changes in expression in cultured human keratinocytes.

In an approach of epidermal differentiation, the expression of pemphigus, bullous pemphigoid, and upper-cytoplasmic epidermal antigens was studied in human keratinocytes in culture. The cells were cultured without feeder cells, dermal tissue, or collagen at an acid pH (5.6--5.8) similar to that of the surface of the skin in vivo. Cell suspensions from fresh trypsinized skin and primary, secondary, and tertiary cultures were tested by indirect immunofluorescence for the presence of each antigen using human sera from patients with pemphigus, bullous pemphigoid, and human sera with antibodies against upper-cytoplasmic antigens. Normal sera and cultured human normal fibroblasts and melanoma cells were used as controls. Pemphigus and pemphigoid antigens were found to be expressed, and synthesized by keratinocytes in vitro. The expression to upper-cytoplasmic antigens decreased with time in culture, and they were absent in secondary or tertiary cultures, while expressed by 45--65% of cells prepared from fresh skin. Both upper-cytoplasmic and pemphigoid antigens can be used to type subpopulations of human epidermal cells; however, these findings suggest that epidermal differentiation in vitro differs from that which occurs in vivo.

Antigens↗

Decreased expression of epidermal cytoplasmic antigens in cultured human keratinocytes.

The expression of upper cytoplasmic (U-CYT) antigens which are expressed only in the superficial layers of the epidermis and are markers of epidermal cell differentiation in vivo and of basement zone (BMZ) antigens reacting with bullous pemphigoid serum was studied in keratinocytes in tissue culture. The cells were cultured at an acid pH (5.6-5.8) similar to that of skin and without feeder cells, dermal tissue, or collagen. It was found that the expression of U-CYT antigens decreased markedly in culture. These antigens were expressed in 45-65% of epidermal cells prepared from fresh skin, but in only 5-10% of cells which had been grown in primary culture over 1 mo, and in no cells in secondary or tertiary culture. By contrast, BMZ antigens continued to be expressed in culture. These antigens were expressed by 20-35% of epidermal cells prepared from fresh tissue and by 15-35% of keratinocytes in primary, secondary or tertiary culture. These findings indicate that U-CYT and BMZ antigens can be used to type subpopulations of human keratinocytes in suspension, and suggest that the differentiation of these cells in vitro differs from that which occurs in vivo.

Antigens↗

[PMN leukocytes chemotaxis: inhibition by thalidomide (author's transl)].

The effects of thalidomide on chemotaxis of normal human peripheral blood PMN leukocytes have been studied in vitro. Chemotaxis factor was generated by interacting normal human serum with zymosan. At concentration of 1, 10 and 100 micrograms/ml, thalidomide failed to inhibit chemotactic factor. Pre-incubation of PMNs with thalidomide caused a marked, dose-independent inhibition of chemotaxis. Random mobility did not appear to be affected. Inhibition of PMN chemotactic ability by thalidomide may account for its ability to improve skin diseases such as aphtosis, discoid lupus erythematosus and other sun-sensitive and/or inflammatory dermatoses.

Chemotaxis, Leukocyte↗

Inhibition of PMN leukocytes chemotaxis by thalidomide.

The effects of thalidomide on chemotaxis of normal human peripheral blood PMN leukocytes have been studied in vitro. The chemotaxis factor was generated by interacting normal human serum with bovine gamma globulin-antibovine-gamma globulin immune complexes. At concentrations of 1, 10, and 100 microgram/ml, thalidomide failed to inhibit the chemotactic factor. At the same concentrations, erythromycin caused a marked inhibition of chemotaxis. Pre-incubation of PMNs with thalidomide or erythromycin caused a marked, dose-independent inhibition of chemotaxis. Random mobility did not appear to be affected. Inhibition of PMN chemotactic ability by thalidomide may account for its ability to improve inflammatory dermatoses, such as aphthosis.

Chemotaxis, Leukocyte↗

[Phospholipid antigens acquired by the young forms of Schistosoma mansoni].

Immunofluorescence studies provide evidence of cardiolipin fixation at the schistosomulum's surface, following incubation with liposomes (cardiolipin-lecithin or cardiolipin-lecithin added with cholesterol). Fixation occurs at 37 degrees C as well as at 0 degree C whether proteins were present or not. Several washes do not remove cardiolipin fixation.

Animals↗

Dermal duct tumor.

A dermal duct tumor which clinically resembled an intradermal nevus and developed on the lower back of a 59-year-old woman is described. The diagnosis could only be reached by microscopic examination. The dermal duct tumor appears to originate from cells with differentiation towards the intradermal portion of the eccrine sweat duct.

Female↗

[Cutaneous reactions to propranolol (author's transl)].

A 17-year-old male patient with eczematous and psoriasiform eruption that developed during long-term therapy with Propanolol (Avlocardyl) has been studied. This eruption disappeared after removal of the drug; oral challenge was soon followed by a vesiculous and bullous eruption of face and extremities; five months later, sun exposure was followed by a severe eczematous eruption in these areas; nails changes were then observed. Most of side-effects of beta-adrenergic blocking drugs have been reported with Practolol: lichenoid, exanthematous, eczematous, psoriasiform rashes; exfoliative dermatitis; oculo-muco-cutaneous reactions; fibrosing polyseritis and drug induced systemic lupus erythematosus manifestations. Adverse effects of other beta-adrenergic blocking agents are less frequent. The pathogenetic mechanism responsible for these adverse reactions is still obscur: these changes might be caused by blockade of the epidermal cells (and T-lymphocytes) beta-receptors, more than by a direct immunologic, allergic or toxic mechanism.

Adolescent↗

[Shulman's syndrome: eosinophilic fasciitis (author's transl)].

A detailed report is made of the clinical, histological, biological manifestations of eosinophilic fasciitis, i. e. the Shulman's syndrome, about a 53-year-old man. An extreme induration of sub-cutaneous tissues from arms, legs and trunk, without involvement of the face and extremities, was associated with severe thickening of deep peri-muscular fascias. Raynaud's phenomenon was absent, as were morpheas and visceral involvement. Results of biopsies studied by standard, electron and I. F. microscopy, revealed sclerosis and cellular infiltrates (lymphocytes, plasma cells, histiocytes and eosinophils) in fascia and muscular septa; no changes were seen in epidermis, dermis or sub-cutaneous fat tissue. An elevated ESR, eosinophilia and hyperimmunoglobulinaemia with high levels of circulating immune complexes were the only biological abnormalities. A good response to systemic corticosteroid therapy was observed. These features were similar to those seen in other cases of eosinophilic fasciitis. The etiology and pathogenesis of the Shulman's syndrome remain unclear. A critical review of the literature suggests that eosinophilic fasciitis should be separated from scleroderma and pseudoscleroderma, although this opinion has been discussed.

Adrenal Cortex Hormones↗

Defective leukocytotaxia and recurrent staphylococcal infecion: deficiency of leukocytotaxia and abnormal granulocytes associated with increase serum IgE levels in an adult with recurrent staphylococcal infection.

A man who was suffering from recurrent staphylococcal infection had antecedent symptoms of severe pruritus. Laboratory investigations showed leukocytosis with eosinophilia, hyperimmunoglobulinemia of all fractions, but particularly of IgE, and a deficiency of cell-mediated immunity on in vivo testing. Phagocytosis and bactericidal activity of polymorphonuclear leukocytes were normal, but a cellular and serum-associated defect in leukocytotaxia was present. Ultrastructural changes were observed in polymorphonuclear leukocytes. Association of impaired leukocytotaxia and elevated levels of IgE is not uncommon. Recurrent bacterial infections in the patient described are probably related to defective chemotaxis.

Aged↗