Startseite » Oct 13 Journal of Neuroscience

Boosting Regulatory T Cells Limits Neuroinflammation in Permanent Cortical Stroke

A study by Arthur Liesz and colleagues, published in the October issue of The Journal of Neuroscience, describes the use of histone deacetylase inhibitors (HDACi) to boost the number and function of regulatory T cells (Treg), a specialised cell population orchestrating the immune reaction after ischemic brain injury.

Neuroinflammation after stroke is an important pathophysiological mechanism leading to secondary brain injury by inflammatory collateral damage. Dr. Liesz and team have previously discovered Treg cells to be the key immunosuppressive cell population modulating the poststroke inflammatory reaction (Liesz et al., Nat Med, 2009). Based on this finding, in the recently published project they investigated therapeutic approaches to exploit and improve the beneficiary effects of Treg cells on poststroke inflammation. By using specific histone deacetylase inhibitors, they achieved to increase the number of Treg cells and boost their immunosuppressive capacity. This reduced the resulting brain lesion volume and improved behavioral deficits by attenuating cerebral production of pro-inflammatory cytokines and activation of encephalitogenic T cells. The main mediator of in this way enhanced Treg cells was the immunosuppressive cytokine IL-10.

These results provide a better understanding for novel immunotherapeutic approaches in brain ischemia and might be translated to a broad range of brain diseases including primary neuroinflammatory and neurodegenerative disorders.

Read the full text article provided by The Journal of Neuroscience here...

 

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Figure: Histogram plots of Treg suppression assay analysis between in vivo DMSO (control) or TsA (HDACi) treated animals. Treg cells from HDACi treated animals were more potent in suppressing responder T cells isolated from untreated naïve mice (fitted peaks of proliferation analysis; x-axis: CFSE fluorescence intensity).