Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance [CD4cre miR-23 clusterTg Tr]
Transcriptomics Dataset
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| Accession | GSE89546 |
| Title | Excessive miR-27 expression impairs regulatory T cell-mediated immunological tolerance [CD4cre miR-23 clusterTg Tr] |
| Description | MicroRNAs (miRNAs) are tightly regulated in the immune system, as aberrant expression of miRNAs often results in hematopoietic malignancies and autoimmune diseases. Previously, elevated levels of miR-27 in T cells isolated from multiple sclerosis patients has been suggested to facilitate disease progression through inhibiting Th2 immunity and promoting pathogenic Th1 responses. Here we demonstrate that while mice with T cell-specific overexpression of miR-27 harbor dysregulated Th1 responses and develop autoimmune pathology, these disease phenotypes are not driven by miR-27 in effector T cells in a cell-autonomous manner but rather resulted from a perturbed regulatory T (Treg) cell compartment. Excessive miR-27 expression in T cells severely impairs Treg cell differentiation. Moreover, Treg cells with exaggerated miR-27-mediated gene regulation exhibit diminished homeostasis and suppressor function in vivo. Mechanistically, miR-27 represses several known as well as previously uncharacterized targets that play critical roles in controlling multiple aspects of Treg cell biology. Collectively, our data show miR-27 functions as a key regulator in Treg cell development and function and suggest that proper regulation of miR-27 is pivotal to safeguard Treg cell-mediated immunological tolerance. |
| Landing Page | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE89546 |
| Repository | Gene Expression Omnibus |
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