The tumor-associated antigen EBAG9 negatively regulates the cytolytic capacity of mouse CD8+ T cells.
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ABSTRACT: CTLs eliminate virus-infected and tumorigenic cells through exocytosis of cytotoxic agents from lytic granules. While insights into the intracellular mechanisms facilitating lytic granule release have been obtained through analysis of loss-of-function mutations in humans and mice, there is a paucity of information on negative regulators of secretory lysosome release at the molecular level. By generating and analyzing estrogen receptor-binding fragment-associated antigen 9-KO (Ebag9 KO) mice, we show here that loss of EBAG9 confers CTLs with enhanced cytolytic capacity in vitro and in vivo. Although loss of EBAG9 did not affect lymphocyte development, it led to an increase in CTL secretion of granzyme A, a marker of lytic granules. This resulted in increased cytotoxicity in vitro and an enh
SUBMITTER: Ruder C
PROVIDER: S-EPMC2719940 | biostudies-literature | 2009 Aug
REPOSITORIES: biostudies-literature
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