The earliest T lineage-committed cells depend on IL-7 for Bcl-2 expression and normal cell cycle progression.
Interleukin-7 (IL-7)-deficient mice exhibit an early defect in lymphopoiesis. We examined Bcl-2 expression and the cell cycle status of immature thymocyte subsets in these mice. In IL-7-deficient mice, developmental transition to a T cell-committed fate was accompanied by a striking loss of Bcl-2 protein expression and an increased relative proportion of cells in the G0/G1 stage of the cell cycle. Short-term culture of immature thymocytes with rIL-7 caused up-regulation of Bcl-2 protein and cell survival. These data specify a T cell lineage developmental transition point, prior to T cell antigen receptor rearrangement, where IL-7 signal transduction is linked to an anti-apoptosis mechanism and the cell cycle.
von Freeden-Jeffry
U
U
Department of Immunobiology, DNAX Research Institute, Palo Alto, California 94304, USA.
Solvason
N
N
Howard
M
M
Murray
R
R
D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D015329:Gene Rearrangement, T-Lymphocyte; D015851:Interleukin-7 / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000166:cytology* / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology
D015851:Interleukin-7; D019253:Proto-Oncogene Proteins c-bcl-2; D011948:Receptors, Antigen, T-Cell