Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Transforming growth factor β (TGF-β), an immunomodulator, has inhibitory as well as stimulatory effects on bone marrow cells. In this study, we demonstrate that TGF-β1 also is a bidirectional modulator of CSF receptor expression on murine bone marrow cells. TGF-β1 up-regulated granulocyte- macrophage (GM)-CSF receptor expression in a time- and dose-dependent manner, with a maximum up-regulation of 64% by 48 h at 20 ng/ml. In contrast, TGF- β1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h. TGF-β1 did not affect G-CSF receptor expression, in agreement with its inability to affect G-CSF-induced proliferation. The CSF receptor modulation induced by TGF-β1 preceded its effects on CSF-stimulated proliferation. The effects of TGF-β on CSF receptor expression were isoform dependent, thus TGF-β3 was a 10-fold more potent inhibitor of both IL-3- induced colony formation and IL-3 receptor expression than TGF-β1, whereas TGF-β1 was a more potent stimulator of GM-CSF-stimulated colonies and GM- CSF receptor expression than TGF-β3. Therefore, the ability of TGF-β to modulate the CSF receptor density/cell and/or the actual number of progenitors expressing CSF receptors directly correlates with the multifunctional effects of TGF-β in hematopoiesis.


Journal article


Journal of Immunology

Publication Date





4534 - 4544