HuR ablation destabilizes Foxp3 mRNA and impairs regulatory T cell function, contributing to an autoimmune phenotype
These findings together suggest that ablation of HuR in Tregs disrupts Foxp3 expression and Treg function, likely through dysregulation of T cell differentiation pathways involving RORγt. This potentially contributes to a disrupted Treg-Th17 axis and autoimmune dysfunction. These data suggest that HuR-mediated post-transcriptional regulation contributes to maintaining Foxp3 expression and immune homeostasis, although compensatory mechanisms such as increased IL-10 expression may also be involved.
Authors
- Sarah Socha
- Joshua Meier (ORCID: https://orcid.org/0000-0001-5934-2097)
- Kristin Bahleda
- Janean E. Holden (ORCID: https://orcid.org/0000-0002-9520-9354)
- Jason S. Ellis
- Fatemeh Fattahi (ORCID: https://orcid.org/0000-0003-0793-3885)
- Francisco Gomez‐Rivera (ORCID: https://orcid.org/0000-0002-8369-3361)
- Ulus Atasoy (ORCID: https://orcid.org/0000-0002-4095-1359)
- Laura Vallance
Institutions
- University of Michigan (US)
- VA Ann Arbor Healthcare System (US)
- Michigan Medicine (US)
- Whitehead Institute for Biomedical Research (US)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-09-26
- DOI
- https://doi.org/10.3389/fimmu.2025.1618677
- Citations
- 1
- Primary Topic
- Immune Cell Function and Interaction
- Type
- article
- Field-Weighted Citation Impact
- 0.80
Funders
- U.S. Department of Health and Human Services
- U.S. Department of Veterans Affairs
- Arak University of Medical Sciences
- National Institutes of Health