SEC23B-dependent COPII Vesicles Regulate T Cell Immunity

The coordinated release of proteins by T cells enables controlled biological responses. While the molecular mechanisms underlying T cell secretion are being increasingly understood, whether the critical ER-to-Golgi trafficking pathway regulates T cell immunity is not known. We utilized mice with a T cell-specific deletion of SEC23B, a core subunit of Coat Protein Complex II (COPII) which drives ER-to-Golgi cargo transport. We found that following activation, SEC23B-deficient T cells display an altered secretome compared to wild-type, which includes reduced secretion of T cell-derived inflammatory mediators, and which is associated with functional ramifications in vitro and in vivo. Together, these data reveal a critical role for the SEC23B-dependent COPII pathway in T cell immunity.