Serine protease inhibitor 2A is a protective factor for memory T cell development
- 15 August 2004
- journal article
- research article
- Published by Springer Nature in Nature Immunology
- Vol. 5 (9) , 919-926
- https://doi.org/10.1038/ni1107
Abstract
An essential event in the development of memory CD8+ T lymphocytes is the escape of progenitors from programmed cell death, but how this is mediated is unclear. Here we report that the gene encoding serine protease inhibitor 2A (Spi2A), an inhibitor of lysosomal executioner proteases dependent on transcription factor NF-κB, is upregulated in memory cell precursors. Spi2A upregulation protected lymphocytic choriomeningitis virus–specific memory progenitors from programmed cell death. Thus, Spi2A promotes the survival of cytotoxic T lymphocytes, allowing them to differentiate into memory CD8 T cells. These findings suggest a model in which commitment to the memory lineage is facilitated by the upregulation of protective genes.Keywords
This publication has 44 references indexed in Scilit:
- Selective expression of the interleukin 7 receptor identifies effector CD8 T cells that give rise to long-lived memory cellsNature Immunology, 2003
- NF- B protects from the lysosomal pathway of cell deathThe EMBO Journal, 2003
- Molecular and Functional Profiling of Memory CD8 T Cell DifferentiationCell, 2002
- Qualitative differences between naïve and memory T cellsImmunology, 2002
- CD4+ T cell effectors can become memory cells with high efficiency and without further divisionNature Immunology, 2001
- Modelling T-cell memory by genetic marking of memory T cells in vivoNature, 1999
- Linear Differentiation of Cytotoxic Effectors into Memory T LymphocytesScience, 1999
- Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient miceNature, 1994
- Cytotoxic lymphocytes require granzyme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cellsCell, 1994
- Tolerance in T-cell-receptor transgenic mice involves deletion of nonmature CD4+8+ thymocytesNature, 1988