作者: SE Jacobsen , FW Ruscetti , CM Dubois , J Lee , TC Boone
DOI: 10.1182/BLOOD.V77.8.1706.1706
关键词: Transforming growth factor, beta 3 、 Endocrinology 、 Internal medicine 、 Transforming growth factor 、 Cell biology 、 Receptor expression 、 TGF beta receptor 2 、 Growth factor receptor inhibitor 、 Receptor 、 Growth factor receptor 、 Biology 、 Transforming growth factor beta
摘要: Transforming growth factor beta (TGF-beta) is a potent and selective inhibitor of early hematopoietic progenitors leukemic cells. The cellular mechanism(s) underlying this antiproliferative effect is, however, currently unknown. In the present study, we demonstrate that TGF-beta inhibits expression granulocyte-macrophage colony stimulating (GM-CSF), interleukin 3 (IL-3), granulocyte-CSF (G-CSF) receptors on murine factor-dependent independent progenitor cell lines without significant change in receptor affinity. A maximum reduction GM-CSF numbers 65% to 77% was observed by 96-hour incubation with TGF-beta. TGF- induced trans-down-modulation prolonged, noncytotoxic but reversible, not due endogenous production GM- CSF. CSF preceded TGF-beta's inhibitory action. addition, ED50 (1 10 pmol/L) for modulatory similar. surface specific, because other proteins (Ly 5 Ly 17) affected treatment, inhibitors (tumor necrosis interferon) did affect expression. These data suggest downregulation cells involves reducing receptors.