Proteomics

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SEC23B-dependent COPII Vesicles Regulate T Cell Immunity


ABSTRACT: 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.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus musculus  

TISSUE(S): Spleen, Lymph Node

DISEASE(S): Not Available

SUBMITTER: Pavan Reddy  

LAB HEAD: Pavan Reddy

PROVIDER: PXD015766 | Pride | 2021-09-08

REPOSITORIES: Pride

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Publications

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

Kim Stephanie S   Khoriaty Rami R   Li Lu L   McClune Madison M   Kalfa Theodosia A TA   Wu Julia J   Peltier Daniel D   Fujiwara Hideaki H   Sun Yaping Y   Oravecz-Wilson Katherine K   King Richard A RA   Ginsburg David D   Reddy Pavan P  

The Journal of clinical investigation 20210101 2


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 secre  ...[more]

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