IL-4-dependent proliferation of BA/F3 cells expressing a growth-negative mutant of the human IL-4 receptor is restored by enforced expression of Bcl-2

• Published in: Journal of leukocyte biology Vol. 59; no. 4; pp. 586 - 590
• Main Authors: Chung, Johanna, Deutsch, Harald H. J., Kalthoff, Frank S.
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01.04.1996
• Subjects: Animals; Antigens, CD - metabolism; Antigens, CD - physiology; apoptosis; Apoptosis - drug effects; Apoptosis - physiology; Cell Cycle - drug effects; Cell Cycle - physiology; Cell Division - drug effects; Cell Division - physiology; Cells, Cultured; Cytokines - biosynthesis; Cytokines - genetics; Gene Expression Regulation - physiology; Genes, myc; growth mediation; Humans; Interleukin-4 - pharmacology; Mice; Mutation; Proto-Oncogene Proteins - biosynthesis; Proto-Oncogene Proteins - metabolism; Proto-Oncogene Proteins - physiology; Proto-Oncogene Proteins c-bcl-2; Receptors, Interleukin - metabolism; Receptors, Interleukin - physiology; Receptors, Interleukin-4; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; supertransfection; Transfection
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.59.4.586

We have studied the regulation of growth and apoptosis in murine BA/F3 cells stably expressing cytoplasmic deletion mutants of the human interleukin‐4 receptor (hIL‐4R). Previously, we showed that BA/F3 cell transfectants expressing a cytoplasmic deletion mutant of the hIL‐4R that lacks the region between Thr(462) and Ala(580), referred to as δR3, fails to proliferate in the presence of hIL‐4. Here we report that supertransfection of δR3‐expressing cells with a constitutively active murine bcl‐2 gene results in prolonged survival of the δR3/bcl‐2 double transfectants in the absence of cytokines. More importantly, however, the constitutive expression of Bcl‐2 restored their capacity to grow permanently with hIL‐4. This may provide an explanation for the discrepancy with previous reports showing growth mediation by hIL‐4R truncated at position 367.