Journal
ONCOTARGET
Volume 7, Issue 26, Pages 39396-39407Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9818
Keywords
ER stress; UPR; Slfn2; quiescence; XBP1; Immunology and Microbiology Section; Immune response; Immunity
Categories
Funding
- ISRAEL SCIENCE FOUNDATION [1275/12]
- ISRAEL CANCER RESEARCH FUND [13/726/RCDA]
- Marie Curie People grant [322006]
- Concern Foundation
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Immunologically naive lymphocytes are kept in a quiescent state until antigen engagement. These quiescent immune cells are characterized by small cell size, lack of spontaneous proliferation and low metabolic rate. Lymphocyte quiescence is actively enforced condition which ensures the preservation of proper differentiation and proliferation capabilities of naive and memory lymphocytes. Previously we described a chemically induced mutation in Schlafen2 (Slfn2), termed elektra, which breaks quiescence and compromises immunity. However, the mechanism by which Slfn2 maintains quiescence remains unknown. Here we demonstrate that elektra T cells display chronic ER stress under steady state conditions. Modulation of ER stress response by depletion of either UPR mediators XBP1 or CHOP, improved viability and partially corrected the developmental abnormalities and proliferation capabilities of elektra T cells. Altogether, our results demonstrate a functional connection between Slfn2 induced quiescence in T cells and ER homeostasis, clarifying a novel mechanism by which immune cell quiescence is maintained.
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