IL-7 enhances the survival and maintains the size of naive T cells

Journal of Immunology

Volumn 167, Issue 12, 2001, Pages 6869-6876

  Rathmell, J C ^a   Farkash, E A ^a   Gao, W ^a   Thompson, C B ^a  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

GLYCOPROTEIN GP 130; INTERLEUKIN 15; INTERLEUKIN 2; INTERLEUKIN 4; INTERLEUKIN 6; INTERLEUKIN 7; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BCL 2; RAPAMYCIN;

ANIMAL CELL; ARTICLE; CELL SIZE; CELL SURVIVAL; CELL VIABILITY; CONTROLLED STUDY; LYMPHOCYTE PROLIFERATION; MITOGENESIS; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; T LYMPHOCYTE;

EID: 0035892899     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.167.12.6869     Document Type: Article

References (40)

1. Molecular thanatopsis: A discourse on the BCL2 family and cell death
2. Tumor necrosis factor receptor and Fas signaling mechanisms
3. BAX-induced cell death may not require interleukin 1 β-converting enzyme-like proteases
4. The apoptosis-necrosis paradox: Apoptogenic proteases activated after mitochondrial permeability transition determine mode of death
5. L regulates the membrane potential and volume homeostasis of mitochondria
6. Defects in the ubiquitin pathway induce easpase-independent apoptosis blocked by Bcl-2
7. Inhibition of Ced-3/ICE-related proteases does not prevent cell death induced by oncogenes, DNA damage, or the Bcl-2 homologue Bak
8. In the absence of extrinsic signals, nutrient utilization by lymphocytes is insufficient to maintain either cell size or viability
9. Effect of haematopoietic growth factor on intracellular ATP levels
10. L prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange
11. L promote growth factor-independent survival through distinct effects on mitochondrial physiology
12. PI3K: Downstream AKT ion blocks apoptosis
13. Mechanisms and consequences of activation of protein kinase B/Akt
14. Phosphoinositide kinases
15. Regulation of Glut l gene transcription by the serine/threonine kinase Aktl
16. TOR, a central controller of cell growth
17. Early lymphocyte expansion is severely impaired in interleukin 7 receptor-deficient mice
18. Lymphopenia in interleukin (IL)-7 gene-deleted mice identifies IL-7 as a nonredundant cytokine
19. Interleukin 4 (IL-4) or IL-7 prevents the death of resting T cells: Stat6 is probably not required for the effect of IL-4
20. + T cells
21. Cytokineinduced survival of activated T cells in vitro and in vivo
22. Survival of naive CD4 T cells: Roles of restricting versus selecting MHC class II and cytokine milleu
23. T lymphocytes need IL-7, but not IL-4 or IL-6 to survive in vivo
24. Interleukin-7 mediates the homeostasis of naive and memory CD8 T cells in vivo
25. Bcl-2 rescues T lymphopoiesis in interleukin-7 receptor-deficient mice
26. -/- mice
27. Interleukin-7 can induce the activation of Jak 1. Jak 3. and Stat5 proteins in murine T cells
28. JAK3 protein tyrosine kinase mediates interleukin-7-induced activation of phosphatidylinositol-3′ kinase
29. Distinct roles of the phosphatidylinositol 3-kinase and STAT5 pathways in IL-7-mediated development of human thymocyte precursors
30. Interleukin-7 induces the association of phosphatidylinositol 3-kinase with the a chain of the interleukin-7 receptor
31. L and Bcl-2 repress a common pathway of cell death
32. The pentose cycle and insulin release in mouse pancreatic islets
33. IL-6 rescues resting mouse T cells from apoptosis
34. + T cells
35. Conversion of Bcl-2 to a Bax-like death effector by caspases
36. Metabolic changes in activated T cells: An NMR study of human peripheral blood lymphocytes
37. Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation
38. Suppression of signalling through transcription factor NF-AT by interactions between calcineurin and Bcl-2
39. Jak3 selectively regulates Bax and Bci-2 expression to promote T-cell development
40. Growth factors can influence cell growth and survival through effects on glucose metabolism