ArticleThe Journal of clinical investigation2021
ER-to-Golgi transport and SEC23-dependent COPII vesicles regulate T cell alloimmunity.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- The vesicle transport gene SEC23A is a novel prognostic indicator and therapeutic target in gastric cancer.Frontiers in oncology · 2026Article
- Potent Inducers of Paraptosis through Electronic Tuning of Hemicyanine Electrophiles.Journal of the American Chemical Society · 2025Article
- ER-associated degradation adapter Sel1L is required for CD8Cell reports · 2024Article
- ER exit in physiology and disease.Frontiers in molecular biosciences · 2024Review
- Nlp-dependent ER-to-Golgi transport.International journal of biological sciences · 2024Article
- The Deubiquitinase OTUD1 Suppresses Secretory Neutrophil Polarization And Ameliorates Immunopathology of Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- New Cases and Mutations inInternational journal of molecular sciences · 2023Article
- Sec23a inhibits the self-renewal of melanoma cancer stem cells via inactivation of ER-phagy.Cell communication and signaling : CCS · 2022Article
- Disease-Associated Factors at the Endoplasmic Reticulum-Golgi Interface.Traffic (Copenhagen, Denmark)Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
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 dyserythropoietic anemia II (CDAII), which results from Sec23b mutation, did not exhibit a similar phenotype. Mechanistic studies demonstrated that unlike murine KO T cells, T cells from patients with CDAII harbor increased levels of the closely related paralog, SEC23A. In vivo rescue of murine KO by expression of Sec23a from the Sec23b genomic locus restored T cell functions. Together, our data demonstrate a critical role for the COPII pathway, with evidence for functional overlap in vivo between SEC23 paralogs in the regulation of T cell immunity in both mice and humans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.