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Cutting edge: abortive proliferation of CD46-induced Tr1-like cells due to a defective Akt/Survivin signaling pathway.

Abstract : T regulatory cell 1 (Tr1) are low proliferating peripherally induced suppressive T cells. Engaging CD3 and CD46 on human CD4+ T cells induces a Tr1-like phenotype. In this study, we report that human Tr1-like cells do not sustain proliferation over time. The weak proliferation of these cells results first from their inability to sustain expression of various cell cycle-associated proteins, to efficiently degrade the inhibitor of cell cycle progression p27/Kip1 and, as a consequence, in their accumulation in the G0-G1 phase. Also, the reduced proliferation of Tr1-like cells results from their increased sensitivity to death as they divide, through a mechanism that is neither Fas-mediated nor Bcl2/Bcl-xL related. Both properties, impaired cell cycle and death sensitivity, are explained by a specific defective activation of Akt that impairs the expression of Survivin. Thus, our results show that CD3/CD46-induced Tr1-like cells die through a process of abortive proliferation.
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https://www.hal.inserm.fr/inserm-00136616
Contributor : Mathias Faure <>
Submitted on : Tuesday, October 28, 2008 - 11:04:20 AM
Last modification on : Friday, June 5, 2020 - 11:18:01 PM
Long-term archiving on: : Tuesday, April 6, 2010 - 10:30:41 PM

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  • HAL Id : inserm-00136616, version 1
  • PRODINRA : 250296
  • PUBMED : 17015676

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Grégory Meiffren, Monique Flacher, Olga Azocar, Chantal Rabourdin-Combe, Mathias Faure. Cutting edge: abortive proliferation of CD46-induced Tr1-like cells due to a defective Akt/Survivin signaling pathway.. Journal of Immunology, Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists, 2006, 177, pp.4957-61. ⟨inserm-00136616⟩

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