ArticleThe Journal of experimental medicine2016
Thymic CD4 T cell selection requires attenuation of March8-mediated MHCII turnover in cortical epithelial cells through CD83.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 74 citations in OpenAlex.
- Review
- UBL3 Participates in the Early Stages of CD83-Dependent CD4European journal of immunology · 2026Article
- Major histocompatibility class II in murine antigen presenting cells is modified with a branched K63 and K11-linked ubiquitin chain.Scientific reports · 2025Article
- CD83 suppresses endogenous March-I-dependent MHC class II ubiquitination, endocytosis, and degradation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Impact of Chitosan Nanoparticles-Coated Dendritic Cell-Based Vaccine as Cancer Immunotherapy.Vaccines · 2025Article
- Thymus Degeneration in Women and the Influence of Female Sexual Hormones on Thymic Epithelial Cells.International journal of molecular sciences · 2025Review
- Mechanism study of ubiquitination in T cell development and autoimmune disease.Frontiers in immunology · 2024Review
- Ubiquitination of Major Histocompatibility Complex II Changes Its Immunological Recognition Structure.International journal of molecular sciences · 2023Article
- MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation.American journal of physiology. Cell physiology · 2023Article
- CCK2-receptor deficiency impairs immune balance by influencing CD4Experimental biology and medicine (Maywood, N.J.) · 2023Article
- The emerging roles of MARCH8 in viral infections: A double-edged Sword.PLoS pathogens · 2023Review
- Regulation of MHC class II and CD86 expression by March-I in immunity and disease.Current opinion in immunology · 2023Review
- CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023Review
- The Monocytic Cell Line THP-1 as a Validated and Robust Surrogate Model for Human Dendritic Cells.International journal of molecular sciences · 2023Article
- CD83 expressed by macrophages is an important immune checkpoint molecule for the resolution of inflammation.Frontiers in immunology · 2023Article
- Thymic epithelial cells require lipid kinase Vps34 for CD4 but not CD8 T cell selection.The Journal of experimental medicine · 2022Article
- Ubiquitin-like protein 3 (UBL3) is required for MARCH ubiquitination of major histocompatibility complex class II and CD86.Nature communications · 2022Article
- Tilting the Balance: Therapeutic Prospects of CD83 as a Checkpoint Molecule Controlling Resolution of Inflammation.International journal of molecular sciences · 2022Review
- Soluble CD83 improves and accelerates wound healing by the induction of pro-resolving macrophages.Frontiers in immunology · 2022Article
- Updating on Roles of HIV Intrinsic Factors: A Review of Their Antiviral Mechanisms and Emerging Functions.Intervirology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deficiency of CD83 in thymic epithelial cells (TECs) dramatically impairs thymic CD4 T cell selection. CD83 can exert cell-intrinsic and -extrinsic functions through discrete protein domains, but it remains unclear how CD83's capacity to operate through these alternative functional modules relates to its crucial role in TECs. In this study, using viral reconstitution of gene function in TECs, we found that CD83's transmembrane domain is necessary and sufficient for thymic CD4 T cell selection. Moreover, a ubiquitination-resistant MHCII variant restored CD4 T cell selection in Cd83(-/-) mice. Although during dendritic cell maturation CD83 is known to stabilize MHCII through opposing the ubiquitin ligase March1, regulation of March1 did not account for CD83's TEC-intrinsic role. Instead, we provide evidence that MHCII in cortical TECs (cTECs) is targeted by March8, an E3 ligase of as yet unknown physiological substrate specificity. Ablating March8 in Cd83(-/-) mice restored CD4 T cell development. Our results identify CD83-mediated MHCII stabilization through antagonism of March8 as a novel functional adaptation of cTECs for T cell selection. Furthermore, these findings suggest an intriguing division of labor between March1 and March8 in controlling inducible versus constitutive MHCII expression in hematopoietic antigen-presenting cells versus TECs.
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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.