Journal
CELL AND BIOSCIENCE
Volume 1, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/2045-3701-1-3
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Funding
- National Cancer Institute SPORE in Cervical Cancer [P50 CA098252]
- NIH [1 RO1 CA115245-01]
- Johns Hopkins University
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Background: MicroRNA (miRNA) molecules are potent mediators of post-transcriptional gene silencing that are emerging to be critical in the regulation of innate and adaptive immunity. Results: Here we report that miR-155-an oncogenic miRNA with important function in the mammalian immune system-is induced in dendritic cells (DCs) upon maturation and potentially attenuates their ability to activate T cells. Biolistic epidermal transfection with DNA encoding miR-155 suppressed the induction of antigen-specific T cell-mediated immunity, whereas reduction of endogenous miR-155 by a partially complementary antisense sequence reversed this effect. Because DCs represent a significant component of epidermal tissue and are among the most potent of antigen-presenting cells, the inhibitory actions of miR-155 could be mediated through this subset of cells. Conclusions: These results suggest that miR-155 may repress the expression of key molecules involved in lymph node migration, antigen presentation, or T cell activation in DCs, and thus forms part of a negative regulatory pathway that dampens the generation of T cell-mediated immune responses. Modulation of miR-155 expression in epidermis therefore represents a potentially promising form of gene therapy for the control of diseases ranging from autoimmunity to cancer and viral infection.
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