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B F Mackler

Publications and source records attributed to B F Mackler.

51 records · Page 3Linked to original sources
PubMed1976

Cytotoxicity responses to melanoma cells by human lymphoid cell subpopulations.

Lymphoid cell subpopulations from normal donors and patients with malignant melanoma were assessed for cytotoxicity. Unfractionated mononuclear cells and T-cells from melanoma patients gave cell-mediated cytotoxic (CMC) responses to melanoma target cells but not to human fibroblasts. These specific CMC responses to melanoma cells were partially inhibited by autologous serum. Non-T-cells and nonrosetting cells from melanoma patients were not directly cytolytic for melanoma target cells; however these same subpopulations were cytotoxic in the presence of autologous serum, which indicated antibody-dependent cell cytotoxic responses. Non-T-cell subpopulations from normal donors were not cytotoxic when incubated with autologous serum. A third cytotoxic mechanism was demonstrated with complement (C3) receptor-activated lymphocytes. From both melanoma patients and normal donors, cells forming rosettes with erythrocyte-antibody-complement were nonspecifically cytotoxic for lung fibroblasts and melanoma target cells, These responses were independent of antibody, since melanoma serum presumably containing antibody to melanoma target cells neither enhanced nor blocked cytotoxicity mediated by C3 receptor-bearing lymphocytes. The results indicated that lymphoid cell subpopulations from the same melanoma patient could express at least three different lymphocyte-mediated cytotoxicity mechanisms against melanoma target cells.

Antibodies↗
PubMed1975

Physicochemical characterization of chemotatic lymphokines produced by human T and B lymphocytes.

Ostensibly pure populations of T and B lymphocytes were separated from peripheral human blood by a sequential rosetting method. These cells, and mononuclear leukocyte (MNL) cell preparations (60 to 85% T cells), were cultured in vitro and the supernatants of these cultures were assayed for chemotactic lymphokine (CTX) activity. B lymphocytes were activated to produce CTX by binding erythrocytes sensitized with antibody and complement (EAC) to their C3 receptors and phytohemagglutinin (PHA) stimulation of isolated T cells was used to produce T cell-derived CTX. Sephadex G-100 gel filtration chromatography of supernatants obtained from T and B cell cultures showed that both cell types produce a CTX of approximate molecular weight 12,500 daltons. This result is identical to that previously obtained in characterizing the CTX produced by buffy coat leukocytes. Isoelectric focusing of lymphocyte supernatants and chemotactically active Sephadex G-100 fractions showed that the CTX produced by B cells and PHA-stimulated MNL contained two peaks of lymphokine activity, a major peak at pH 10.1 and a minor peak at pH 5.6. Additionally, these studies show that the chemotactic complement peptide C5a has an isoelectric point of pH 8.7 and is antigenically distinct from T and B cell-derived CTX, although relatively homogenous by gel filtration, contain two isoelectrically distinct species. In addition, these findings suggest that T and B cells although possessing different membrane receptors and requiring different mechanisms of activation to initiate lymphokine synthesis, produce lymphokines with identical physiocochemical properties.

Animals↗
PubMed1974

Blastogenesis and lymphokine synthesis by T and B lymphocytes from patients with periodontal disease.

Thymus-derived (T) and bone marrow-derived (B) lymphocytes were isolated from human peripheral blood and cultured with various mitogens and antigens. Purified protein derivative of tuberculin stimulated both purified T and B cells from patients with positive skin reactivity to purified protein derivative but did not stimulate nonimmune lymphocytes. Similarly, both T and B lymphocytes from patients with periodontal disease were stimulated to proliferate when incubated with dental plaque, whereas cells from normal individuals without gingivitis were unresponsive. In contrast, one component of plaque, bacterial endotoxins (lipopolysaccharide), minimally stimulated B lymphocytes from both normal or gingivitis patients. T lymphocytes from patients with periodontal disease were also stimulated by plaque antigen to produce chemotactic lymphokine activity (CTX) for human monocytes. B cells purified by the EAC rosetting method nonspecifically produced CTX without concomitant blastogenesis; however, after dissociation of adherent EAC these immune B cells did not spontaneously produce CTX. Lymphokine synthesis by B cells was not dependent on concomitant blastogenesis. Dissociated B cells from periodontitis patients also produced CTX activity after stimulation with dental plaque antigen. Therefore, both T and B lymphocytes, after stimulation with nonendotoxin antigenic components of plaque, proliferated and produced lymphokines, which are presumed to contribute to the pathogenesis of periodontal disease.

Adult↗