ArticleThe Journal of experimental medicine2021
Targeting transcriptional coregulator OCA-B/Pou2af1 blocks activated autoreactive T cells in the pancreas and type 1 diabetes.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Regulation of B cell development and lymphocyte function by transcriptional coactivator OCA-B.Frontiers in immunology · 2026Review
- OCA-B promotes pathogenic maturation of stem-like CD4+ T cells and autoimmune demyelination.The Journal of clinical investigation · 2025Article
- Transcriptional co-regulator OCA-B/Pou2af1 restricts Th2 differentiation.Frontiers in immunology · 2025Article
- OCA-B/Pou2af1 is sufficient to promote CD4Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Bob1 maintains T follicular helper cells for long-term humoral immunity.Communications biology · 2024Article
- Deficiency of Trex1 leads to spontaneous development of type 1 diabetes.Nutrition & metabolism · 2024Article
- A novel iTreg-related signature for prognostic prediction in lung adenocarcinoma.Cancer science · 2024Article
- Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes.Cell & bioscience · 2023Review
- WDFY4 deficiency in NOD mice ameliorates autoimmune diabetes and insulitis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- T Cell Specific BOB.1/OBF.1 Expression Promotes Germinal Center Response and T Helper Cell Differentiation.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
The transcriptional coregulator OCA-B promotes expression of T cell target genes in cases of repeated antigen exposure, a necessary feature of autoimmunity. We hypothesized that T cell-specific OCA-B deletion and pharmacologic OCA-B inhibition would protect mice from autoimmune diabetes. We developed an Ocab conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell-specific OCA-B loss protected mice from spontaneous disease. Protection was associated with large reductions in islet CD8+ T cell receptor specificities associated with diabetes pathogenesis. CD4+ clones associated with diabetes were present but associated with anergic phenotypes. The protective effect of OCA-B loss was recapitulated using autoantigen-specific NY8.3 mice but diminished in monoclonal models specific to artificial or neoantigens. Rationally designed membrane-penetrating OCA-B peptide inhibitors normalized glucose levels and reduced T cell infiltration and proinflammatory cytokine expression in newly diabetic NOD mice. Together, the results indicate that OCA-B is a potent autoimmune regulator and a promising target for pharmacologic inhibition.
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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.