Abbreviated Journal Title
cytokine; proliferation; lymphocytes; homeostasis; metabolism; T-CELL PROLIFERATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; RECEPTOR-DEFICIENT; MICE; SEVERE COMBINED IMMUNODEFICIENCY; SIGNAL-TRANSDUCTION; CYCLE; PROGRESSION; PHOSPHATIDYLINOSITOL 3-KINASE; LYMPHOID DEVELOPMENT; SURVIVAL SIGNALS; GENE-EXPRESSION; Biochemistry & Molecular Biology; Cell Biology; Immunology
The signaling processes that maintain the homeostatic proliferation of peripheral T-cells and result in their self-renewal largely remain to be elucidated. Much focus has been placed on the anti-apoptotic function of the cytokine, interleukin-7 (IL-7), during T-cell development. But a more critical role has been ascribed to IL-7 as a mediator of peripheral T-cell maintenance. The biological effects responsive to IL-7 signaling are transduced through only a few well-known pathways. In this review we will focus on the signals transduced by IL-7 and similar cytokines, examining how proliferative signals originate from cytokine receptors, are amplified and eventually alter gene expression. In this regard we will highlight the crosstalk between pathways that promote survival, drive cell cycle progression and most importantly provide the needed energy to sustain these critical cellular activities. Though this review showcases much of what has been learned about IL-7 proliferative signaling, it also reveals the significant gaps in our knowledge about cytokine signaling in the very relevant context of peripheral T-cell homeostasis. (C) 2007 Elsevier Ltd. All rights reserved.
"Interfinking interleukin-7" (2007). Faculty Bibliography 2000s. 7304.