ER-to-Golgi transport and SEC23-dependent COPII vesicles regulate T cell alloimmunity.

ABSTRACT: T cell-mediated responses are dependent on their secretion of key effector molecules. However, the critical molecular determinants of the secretion of these proteins are largely undefined. Here, we demonstrate that T cell activation increases trafficking via the ER-to-Golgi pathway. To study the functional role of this pathway, we generated mice with a T cell-specific deletion in SEC23B, a core subunit of coat protein complex II (COPII). We found that SEC23B critically regulated the T cell secretome following activation. SEC23B-deficient T cells exhibited a proliferative defect and reduced effector functions in vitro, as well as in experimental models of allogeneic and xenogeneic hematopoietic cell transplantation in vivo. However, T cells derived from 3 patients with congenital dyserythro

SUBMITTER: Kim S 

PROVIDER: S-EPMC7810489 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature