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Regulation of human blood erythroid burst forming unit proliferation by t lymphocyte sub populations defined by fc receptors and mono clonal antibodies


, : Regulation of human blood erythroid burst forming unit proliferation by t lymphocyte sub populations defined by fc receptors and mono clonal antibodies. Blood 59(5): 990-996

To determine whether normal T-cell subpopulations influence human blood BFU-E [erythropoietic burst-forming cell] proliferation variably, sheep erythrocyte rosettable cells (unseparated T cells) were fractionated into subpopulations based on their differential binding to IgM (T.mu. cells) or IgG-coated ox erythrocytes (T.gamma. cells). For comparative purposes, T cells, T.gamma. cells and T cells depleted of T.gamma. cells (T-non-.gamma. cells) were further characterized by their reaction with the OK [hybridoma derived] panel of monoclonal antibodies (OKT3, OKT4, OKT8, OKM1). Quantities of 2.0 .times. 105 T.mu., T.gamma. or T-non-.gamma. cells were mixed with 2.0 .times. 105 autologous BFU-E-enriched null cells in a methyl-cellulose culture system with 2.0 IU erythropoietin. T.mu. cells or T-non-.gamma. cells consistently increased BFU-E numbers above that observed with either unseparated T cells or T.gamma. cells (P < 0.005, n = 10). The differential burst-enhancing effect of T.mu. and T.gamma. cells was evident in increasing cell numbers in culture and in mixing studies. T.gamma. cells in the absence or presence of mitogens did not consistently suppress BFU-E growth below that observed in cultures with null cells alone. Monoclonal antibody analysis of T-cell subsets indicated that T.gamma. cells were enriched for OKM1+ cells and reduced in OKT3+, OKT4+ cells as compared to unseparated T cells or T-non-.gamma. cells (P < 0.05). T-non-.gamma.-cells were enriched for OKT3, OKT4+ cells and were depleted of OKM1+ cells (P < 0.05). OKT8 positivity of these cell fractions was similar. Treatment of unseparated T cells with OKT4 antibody plus complement significantly reduced the BFU-E enhancing effects of these T cells compared to complement-treated controls (P 0.005). These studies provide direct evidence for the concept of T-cell subset regulation of erythropoiesis. The variable burst-enhancing effects of T.mu., T-non-.gamma. and T.gamma. cells may be due to the presence of variable numbers of a burst-enhancing OKT4+ cell. The possibility that the differential BFU-E stimulatory effect of T.mu. or T.gamma. cells is due to cellular interactions with monocytes is not excluded by these studies.

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