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The Pim kinases control rapamycin-resistant T cell survival and activation
Open accessAbstract
Although Pim-1 or Pim-2 can contribute to lymphoid transformation when overexpressed, the physiologic role of these kinases in the immune response is uncertain. We now report that T cells from Pim-1−/−Pim-2−/− animals display an unexpected sensitivity to the immunosuppressant rapamycin. Cytokine-induced Pim-1 and Pim-2 promote the rapamycin-resistant survival of lymphocytes. The endogenous function of the Pim kinases was not restricted to the regulation of cell survival. Like the rapamycin target TOR, the Pim kinases also contribute to the regulation of lymphocyte growth and proliferation. Although rapamycin has a minimal effect on wild-type T cell expansion in vitro and in vivo, it completely suppresses the response of Pim-1−/−Pim-2−/− cells. Thus, endogenous levels of the Pim kinases are required for T cells to mount an immune response in the presence of rapamycin. The existence of a rapamycin-insensitive pathway that regulates T cell growth and survival has important implications for understanding how rapamycin functions as an immunomodulatory drug and for the development of complementary immunotherapeutics.
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Cites
Structural biology of the Bcl-2 family of proteins
Petros, A. M., Olejniczak, E. T., & Fesik, S. W. (2004) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2003.08.012 · Cited by 745
Cited by
Fuel feeds function: energy metabolism and the T-cell response
Fox, C. J., Hammerman, P. S., & Thompson, C. B. (2005) · Nature Reviews Immunology · doi:10.1038/nri1710 · Cited by 853
Self-citationRegulation of Immune Responses by mTOR
Powell, J. D., Pollizzi, K. N., Heikamp, E. B., & Horton, M. R. (2012) · Annual Review of Immunology · doi:10.1146/annurev-immunol-020711-075024 · Cited by 836
Wellen, K. E., Lu, C., Mancuso, A., Lemons, J. M. S., Ryczko, M., Dennis, J. W., Rabinowitz, J. D., Coller, H. A., & Thompson, C. B. (2010) · Genes & Development · doi:10.1101/gad.1985910 · Cited by 377
Self-citationMcCubrey, J. A., Steelman, L. S., Chappell, W. H., Abrams, S. L., Franklin, R. A., Montalto, G., Cervello, M., Libra, M., Candido, S., Malaponte, G., et al. (2012) · Oncotarget · doi:10.18632/oncotarget.659 · Cited by 314
Malone, T., Schäfer, L., Simon, N., Heavey, S., Cuffe, S., Finn, S., Moore, G., & Gately, K. (2020) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2019.107454 · Cited by 33
Metadata
- Authors
- Fox, C. J., Hammerman, P. S., & Thompson, C. B.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2005-01-10
- Volume
- 201
- Issue
- 2
- Pages
- 259-266
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2166318113
- Cited by
- 185
- References
- 1
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Fox, C. J., Hammerman, P. S., & Thompson, C. B. (2005). The Pim kinases control rapamycin-resistant T cell survival and activation. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20042020
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