Modulation of Endoplasmic Reticulum Stress Controls CD4⁺ T-cell Activation and Antitumor Function.

ABSTRACT: The endoplasmic reticulum (ER) is an energy-sensing organelle with intimate ties to programming cell activation and metabolic fate. T-cell receptor (TCR) activation represents a form of acute cell stress and induces mobilization of ER Ca²⁺ stores. The role of the ER in programming T-cell activation and metabolic fate remains largely undefined. Gp96 is an ER protein with functions as a molecular chaperone and Ca²⁺ buffering protein. We hypothesized that the ER stress response may be important for CD4⁺ T-cell activation and that gp96 may be integral to this process. To test our hypothesis, we utilized genetic deletion of the gp96 gene Hsp90b1 in a CD4⁺ T cell-specific manner. We show that gp96-deficient CD4⁺ T cells cannot undergo

SUBMITTER: Thaxton JE 

PROVIDER: S-EPMC5585019 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature