Send to

Choose Destination
Arthritis Rheum. 2013 Jul;65(7):1882-90. doi: 10.1002/art.37966.

Glucocorticoids suppress T cell function by up-regulating microRNA-98.

Author information

Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.



To identify microRNAs (miRNAs) in human T cells that can explain known antiinflammatory properties of steroids.


Activated human CD4+ T cells from healthy donors were exposed to 1 μM methylprednisolone (MP) in vitro and then subjected to miRNA and messenger RNA microarray analyses. Changes in expression profiles were recorded. Using quantitative polymerase chain reaction (qPCR), flow cytometry, and enzyme-linked immunosorbent assay (ELISA), we confirmed the suppression of predicted targets, and through miRNA transfection experiments, we could suggest mechanistic links.


We identified numerous steroid-responsive genes and miRNAs-many known and some novel-including multiple previously unknown proinflammatory genes suppressed by MP. Further studies using qPCR, flow cytometry, and ELISA demonstrated that methylprednisolone increased the expression of miRNA-98 (miR-98) and suppressed the levels of predicted targets, including interleukin-13 and 3 tumor necrosis factor receptors (TNFRs): Fas, FasL, and TNFR superfamily member 1B. Forced expression of miR-98 in T cells resulted in suppression of the same targets.


The findings of this study demonstrate a link between miR-98 expression and the effects of MP and provide evidence suggesting that MP acts through miR-98 to inhibit specific proinflammatory targets. Identification of this antiinflammatory mechanism of glucocorticoids is important, since it may pave the way toward the elusive goal of dissociating adverse effects from therapeutic effects.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center