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The Journal of Immunology, Vol 157, Issue 11 4926-4934, Copyright © 1996 by American Association of Immunologists
ARTICLES |
J Zamorano, HY Wang, LM Wang, JH Pierce and AD Keegan
Immunology Department, Jerome Holland Laboratories, American Red Cross, Rockville, MD 20855, USA.
Although it has been known for some time that IL-4 protects cells from death via apoptosis, very little is known about the mechanism by which IL-4 exerts this effect. In this report, we have studied the molecular mechanisms of the IL-4-induced prevention of apoptosis in the 32D and B cell systems. IL-3 withdrawal has been shown to induce G1-arrest in 32D cells and subsequent death by apoptosis. We found that overexpression of IRS-1 protected 32D cells from death induced by IL-3 deprivation. IL- 4 was able to protect 32D cells from apoptosis in the presence or absence of IRS-1. However, the protection from apoptosis of cells cultured in IL-4 was greater in the presence of IRS-1 and it reached levels comparable to those of cells cultured in IL-3. The IRS-1- dependent prevention of apoptosis is linked to the activation of PI 3'- kinase since wortmannin and LY294002, two inhibitors of PI 3'-K, partially inhibited the prevention of apoptosis mediated by IL-4 in 32D- IRS-1 cells after IL-3 withdrawal but not in 32D cells lacking IRS-1 expression. In addition, we found that the IRS/PI 3'-K pathway is, at least in part, responsible for the prevention of apoptosis by IL-4 in normal splenic B cell cultures. In spite of the ability of murine IL-4 to partially protect 32D cells lacking IRS-1 from apoptosis, human IL-4 was not able to prevent cell death in 32D-IRS-1 cells transfected with the human IL-4 receptor mutated in the insulin-lL-4 receptor motif (14R- motif) at amino acid 497 (Y497F). This mutation has previously been shown to abrogate the tyrosine phosphorylation of IRS-1 by human IL-4. These results demonstrate that IL-4 protects 32D cells from apoptosis by two different pathways, one of them mediated by IRS-1. In addition, these results suggest that the 14R-motif of the IL-4R is linked to both pathways.
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J. Zamorano and A. D. Keegan Regulation of Apoptosis by Tyrosine-Containing Domains of IL-4R{alpha}: Y497 and Y713, But Not the STAT6-Docking Tyrosines, Signal Protection from Apoptosis J. Immunol., July 15, 1998; 161(2): 859 - 867. [Abstract] [Full Text] [PDF]
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H. Y. Wang, J. Zamorano, and A. D. Keegan A Role for the Insulin-Interleukin (IL)-4 Receptor Motif of the IL-4 Receptor alpha -Chain in Regulating Activation of the Insulin Receptor Substrate 2 and Signal Transducer and Activator of Transcription 6 Pathways. ANALYSIS BY MUTAGENESIS J. Biol. Chem., April 17, 1998; 273(16): 9898 - 9905. [Abstract] [Full Text] [PDF]
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J. Zamorano, H. Y. Wang, R. Wang, Y. Shi, G. D. Longmore, and A. D. Keegan Regulation of Cell Growth by IL-2: Role of STAT5 in Protection from Apoptosis But Not in Cell Cycle Progression J. Immunol., April 1, 1998; 160(7): 3502 - 3512. [Abstract] [Full Text] [PDF]
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F. Bertrand, A. Atfi, A. Cadoret, G. L'Allemain, H. Robin, O. Lascols, J. Capeau, and G. Cherqui A Role for Nuclear Factor kappa B in the Antiapoptotic Function of Insulin J. Biol. Chem., January 30, 1998; 273(5): 2931 - 2938. [Abstract] [Full Text] [PDF]
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D. Wang, J. Zamorano, A. D. Keegan, and M. Boothby HMG-I(Y) Phosphorylation Status as a Nuclear Target Regulated through Insulin Receptor Substrate-1 and the I4R Motif of the Interleukin-4 Receptor J. Biol. Chem., October 3, 1997; 272(40): 25083 - 25090. [Abstract] [Full Text] [PDF]
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B. Valentinis, M. Navarro, T. Zanocco-Marani, P. Edmonds, J. McCormick, A. Morrione, A. Sacchi, G. Romano, K. Reiss, and R. Baserga Insulin Receptor Substrate-1, p70S6K, and Cell Size in Transformation and Differentiation of Hemopoietic Cells J. Biol. Chem., August 11, 2000; 275(33): 25451 - 25459. [Abstract] [Full Text] [PDF]
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