Receptor-specific inhibition of bone marrow erythropoiesis by recombinant DNA-derived XXXX .

@entity3647 @entity1619 @entity5041 @entity379 @entity1199
@entity1199 ( @entity1199 ) induces differential secretion of lymphokines by @entity3647 ( @entity3647 )-positive and @entity3647 -negative T cells. We studied T cell @entity3647 -specific modulation of adult bone marrow erythropoiesis by recombinant @entity1199 ( @entity5041 ). I3-2R were induced by CD3 T cell surface determinant-triggering and analyzed by cytofluorography. Bone marrow monocyte and T cell-depleted ( @entity1619 ) target cells were assessed for early erythroid progenitor expression (BFU-E) in the presence of 0 to 10(3) U/mL of @entity5041 , @entity5041 had no significant effect on BFU-E expression in the absence of T cells or in the presence of @entity3647 -negative T cells. @entity5041 caused a dose-dependent inhibition (75% to 90%) of BFU-E in the presence of autologous @entity3647 -positive T cells. The addition of anti- @entity3647 antibody to cultures containing @entity5041 plus @entity3647 -positive T cells entirely abrogated @entity5041 -mediated inhibition of BFU-E. In the presence of @entity5041 (10(2) U/mL) production of @entity379 ) by adult marrow CD3-triggered @entity3647 -positive T cells was increased 37- to 125-fold compared to @entity3647 -negative T cells. rIF-gamma caused a dose-dependent (88% +/- 17% at 10(3) U/mL) inhibition of adult BFU-E in the presence of CD3-triggered autologous T cells. @entity5041 -mediated inhibition of adult BFU-E in the presence of @entity3647 -positive T cells was partially abrogated (52% +/- 16%) following addition of monospecific IF-gamma antibody. These results demonstrate (a) @entity5041 modulation of adult marrow erythropoiesis is selectively dependent upon both the presence or absence of autologous T cells and the @entity3647 status of these T cells; and (b) @entity5041 -induced inhibition of adult marrow erythropoiesis is mediated in part by release of IF-gamma from @entity3647 -positive T cells.
