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Correlation between the growth‐inhibitory effect of TGF‐β1 and phenotypic characteristics in a panel of B‐cell lines
Author(s) -
Altiok Aysin,
EhlinHenriksson Barbro,
Klein Eva
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910550124
Subject(s) - phenotype , cell culture , biology , in vitro , somatic cell , microbiology and biotechnology , b cell , immortalised cell line , cell , transforming growth factor beta , lymphoma , epstein–barr virus , transforming growth factor , genetics , immunology , gene , virus , antibody
Human B‐cell lines established from Burkitt lymphoma (BL) and normal B cells immortalized in vitro by EBV (LCLs) differ in phenotype. While the BL correspond to resting B cells, the LCLs resemble activated B cells. When BLs which have the EBV genome are carried in vitro , they acquire some of the features of LCLs, such as expression of B‐cell activation markers and the tendency to form aggregates. Comparison of several B‐cell lines for sensitivity to TGF‐β showed that the growth of BLs (with few exceptions), but not of the LCLs, was inhibited. The results suggested that the sensitivity to TGF‐β correlates with the cellular phenotype. In the present work, this assumption is even more critically substantiated by studying 2 sublines of an EBV‐genome carrying BL line, Mutu, which were selected for single cells and aggregates. The former (with resting phenotype) was inhibited, while the subline of aggregated cells, which also expressed B‐cell activation markers, was not inhibited. Somatic‐cell hybrids between BLs, LCLs and non‐B cells provided lines with phenotypic differences. Results with a panel of such hybrid lines also showed that those which express the activated B‐cell phenotype are not inhibited by TGF‐β. Differences in the levels of expression of activation markers did not influence the response to TGF‐β. © 1993 Wiley‐Liss, Inc.