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Biomedical subjects

J J Ballet

Publications and source records attributed to J J Ballet.

At least 91 records · Page 5Linked to original sources

Parasite-derived mitogenic activity for human T cells in Plasmodium falciparum continuous cultures.

Supernatants from Plasmodium falciparum continuous cultures exhibited mitogenic activity against human blood lymphocytes from unsensitized donors. This effect, which was not observed with supernatants from control cultures grown in the absence of the parasites, was dependent upon (i) the concentration of supernatant added to the lymphocyte cultures and (ii) the parasite concentration in the P. falciparum continuous cultures. T cells were the predominant target cells of this mitogenic activity. We observed similar response in lymphocytes from malaria-sensitized individuals to P. falciparum continuous culture material. We also detected a mitogenic activity in parasite-infected erythrocytes from P. falciparum continuous cultures. P. falciparum continuous cultures may provide practical quantities of parasite-derived substances which, presumably, are able to manipulate the immune effector mechanisms of an infected host.

Animals↗

Reactivity of human lymphoid and lymphoblastoid cells with peanut agglutinin: detection of a blood cell subset which lacks detectable membrane HLA.

The number of cells reacting with fluorescein-labelled peanut agglutinin varies widely among human lymphoid organs. By separation techniques, reactive cells from tonsils were characterized as E-negative, non-immunoglobulin-bearing lymphocytes. In peripheral blood, the lectin reacted with a small percentage of lymphoid and monocytoid cells which lacked HLA membrane determinants but expressed the beta 2-microglobulin antigens. The latter phenotype was also found on human lymphoblastoid cell lines. Lectin binding thus provides an effective means of characterizing these cell subsets.

Antigen-Antibody Reactions↗

Impaired defense against vaccinia in a child with T-lymphocyte deficiency associated with inosine phosphorylase defect.

A case of progressive vaccinia associated with a profound deficiency of cellular immunity and a defect in inosine phosphorylase is described. A striking contrast was observed between humoral immunity, which showed little if any impairment, and a severe cellular defect affecting both markers and functions of T lymphocytes. The child died despite treatment with methosazone, levamisole, transfer factor, irradiated blood transfusions, and a thymus graft. An adequate serum level of antibody to vaccinia virus was obtained by transfer of specific immunoglobulins, but this failed to stop the progression of the disease. This observation suggests that host defense against vaccinia infection is mainly mediated by cellular immunity.

Animals↗

Selective defect of precursor T cells associated with apparently normal B lymphocytes in severe combined immunodeficiency disease.

Two patients, one with an autosomal and the other a sex-linked form of severe combined immunodeficiency, had more than 95% B cells in their peripheral blood. Despite an increased absolute number of B lymphocytes, the patients were unable to produce serum antibodies. In each patient, geno- or pheno-identical bone marrow transplantation was followed by the visualization of a thymus shadow and the appearance of both cellular and humoral functions. Chromosome of allotype studies showed that the T cell originated from the donor whereas serum immunoglobulins were synthesized by host B cells. In these patients the pathogenesis appears to be a selective defect of bone marrow precursor T cells without concomitant intrinsic B cell defect. The successful outcome of the graft in these two patients, who are now, respectively, 5 years and 11 months of age and free of infections, indicates that the preferred form of therapy in such patients is transplantation of bone marrow stem cells, which populate the thymus and mature slowly into T cells that cooperate fully with host B cells in synthesis of antibody.

B-Lymphocytes↗

Specific inhibition of in vitro Candida-induced lymphocyte proliferation by polysaccharidic antigens present in the serum of patients with chronic mucocutaneous candidiasis.

A specific inhibitory activity of in vitro proliferative responses of normal human lymphocytes to Candida metabolic antigen was found in the serum of 6 out of 23 children with chronic mucocutaneous candidiasis. In each of the six patients, the presence of an inhibitory activity was associated with Candida-specific cellular defects, characterized by a negative-skin test and a lack of in vitro lymphocyte proliferation. The presence of a circulating inhibitor was detected during relapses of the disease and disappeared under antifungal therapy. This inhibitory effect was not associated with any toxicity on tested lymphocytes. The factor was shown to be nondialysable, thermostable, nonprecipitable with ammonium sulfate and absorbable on anti-Candida antibodies or concanavalin A-coupled agarose columns. Altogether, these results suggest that the inhibitory factor is not an immunoglobulin, but rather a polysaccharidic antigen of Candida albicans. An inhibition of Candida-induced proliferative response of normal human lymphocytes was also obtained by addition of polysacharide antigens or purified mannans from C. albicans to cultures. Candida polysaccharidic antigens appeared, therefore, to be involved in specific depression of cellular functions observed in chronic candidiasis.

Adolescent↗

Inhibition of maturation of human precursor lymphocytes by coformycin, an inhibitor of the enzyme adenosine deaminase.

High concentrations of adenosine are known to be toxic to fibroblasts and lymphocytes under conditions of in vitro culture (1,2). Normally, accumulation of adenosine nucleotides in all mammalian cells is prevented by the presence of adenosine deaminase, an aminohydrolase which converts adenosine to inosine (3). A genetically determined deficiency of adenosine deaminase has been associated with the autosomal recessive form of severe combined immunodeficiency, a syndrome in which precursor lymphocytes fail to mature into T cells and B cells (4-7). Erythrocytes of affected infants convert exogenous adenosine to AMP and ATP at an abnormally increased rate as a consequence of the enzyme defect, and ATP at an abnormally increased rate as a consequence of the enzyme defect, and fail to form inosine from the exogenous adenosine (8). These metabolic disturbances can be mimicked in normal erythrocytes by coformycin (8), a potent competitive inhibitor of adenosine deaminase (9, 10). In this study, the effects of coformycin were examined on the in vitro function of normal lymphocytes.

Adenosine Deaminase Inhibitors↗