Researchers at the University of South Florida have developed a novel use of an miRNA142 to regulate the differentiation of a het-erogeneous group of cells termed as myeloid derived suppressor cells (MDSCs). These cells are known to accumulate in pathological condi-tions like cancers, infections and non -infectious triggers that elicit an in-flammatory signal.
Inflammation underlies the genesis of multiple human disease including cancer, cardiovascular, infectious and neurological conditions. It involves a well-orchestrated group of cytokines and cellular events from an acute to a chronic stage. Prolonged inflammatory condition leads to accumulation of MDSC, which in elderly humans can lead to an immune suppressed states that is referred to an immune senescence.
It has been shown that overexpression of miRNA-142 in MDSCs is suffi-cient to differentiate them into antigen -presenting cells. Also, miRNA -142-overexpressing Tg mice lack MDSC expansion, suggesting that therapeutic overexpression of miRNA-142 can induce MDSC differentiation and cor-rect defective immunity. It is then believed that therapeutic intervention to alter the differentiation of MDSCs can modulate chronic inflammation.
Our inventors have proposed an axis of Chronic Lung Inflammation (CLI) involving miRNA-regulated expression of IL-6 in MDSCs (MIM axis of CLI) that initiates a self -perpetuating inflammatory cascade. This targeted de-livery of miRNA-nanoparticles to MDSCs to redirect differentiation and alter immunity from ‘suppressor’ to ‘responder’ mode may be harnessed to develop novel therapeutics for chronic lung inflammation in the elderly.
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