Biphasic effect of transforming growth factor-beta on Epstein-Barr virus-induced activation of human tonsillar B cells.
Transforming growth factor-beta (TGF-beta) is known to inhibit mitogen-induced proliferation of human B lymphocytes. Earlier results showed that activation of B cells by Epstein-Barr virus (EBV) was also inhibited by TGF-beta. On the other hand, TGF-beta could enhance the transformation of EBV-infected B-cell cultures. In the present set of experiments, we have confirmed the inhibitory effect of TGF-beta on the EBV-induced blastogenesis and found lower expression of CD23 in the treated cultures. However, cells which escaped inhibition and entered in the blast stage expressed a higher level of CD23 molecules. The elevation of CD23 in the TGF-beta-treated cultures was more marked at a time when the cell size profiles of the control and treated cultures were similar. In view of the function of the CD23 molecule as an autocrine growth factor, its increased expression is consistent with previous findings on TGF-beta-mediated enhancement of the transformation of B-cell cultures. The occurrence of growth inhibitory and growth stimulatory effect of TGF-beta on the same cell type has been observed in several other systems as well.
Altiok
A
A
Microbiology and Tumorbiology Center (MTC), Karolinska Institute, Stockholm, Sweden.
Jädersten
M
M
Magyarlaki
T
T
Klein
E
E
D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D005434:Flow Cytometry; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects*; D014066:Palatine Tonsil / Q000166:cytology; D017455:Receptors, IgE / Q000096:biosynthesis; D016212:Transforming Growth Factor beta / Q000494:pharmacology*
D017455:Receptors, IgE; D016212:Transforming Growth Factor beta