Abstract
MicroRNAs (miRNAs), a class of small non-coding RNAs of 18–24 nucleotides in length, function to posttranscriptionally regulate protein expression. miR-155 was one of the first identified and, to date, the most studied miRNA, and has been linked to various cellular processes such as modulation of immune responses and oncogenesis. Previous studies have identified miR-155 as a crucial positive regulator of Th1 immune response in autoimmune diseases, but as a suppressor of Th2 immunity in allergic disorders. However, recent studies have found new evidence that miR-155 plays an indispensible role in allergic asthma. This review summarizes the recent findings with respect to miR-155 in immune responses and the underlying mechanisms responsible for miR-155-related allergic diseases, as well as the similarities between miR-155 and glucocorticoids in immunity.
Highlights
MicroRNAs are a class of naturally-occurring small non-coding RNAs 18–24 nucleotides in length [1] and function to post-transcriptionally inhibit expression of their target mRNAs in cells by binding to the 3 -untranslational region of mRNAs, thereby suppressing translation or promoting mRNA degradation [2]
The functional single strand RNA is further dissociated from the non-functional one and assembled into RNA-induced silencing complex (RISC), which is comprised of various proteins, including Argonaute and Dicer, to target and suppress mRNAs with the RISC [4]. miRNA nucleotide sequences do not always have to precisely complementarily correspond to sequences of their target mRNAs, and one miRNA molecule has an ability to bind to various targeting mRNAs [5], indicating the diversity of gene expression regulation
The involvement of miRNAs in human cancer first became evident from a study of chromosomal 13q14 deletion in human chronic lymphocytic leukemia (CLL), which revealed that miR-15a and miR-16-1 were downregulated in 50%–60% of human CLL cases [10]
Summary
MicroRNAs (miRNAs) are a class of naturally-occurring small non-coding RNAs 18–24 nucleotides in length [1] and function to post-transcriptionally inhibit expression of their target mRNAs in cells by binding to the 3 -untranslational region of mRNAs, thereby suppressing translation or promoting mRNA degradation [2]. In vitro culture of miR-155 KO CD4+ T cells with IL-4 stimulation resulted in enhanced Th2 differentiation, accompanied by elevated levels of Th2 cytokines (such as IL-4, IL-5, and IL-10), indicating that miR-155 may negatively regulate Th2 immune responses and inhibit the occurrence of inflammation in allergic diseases [21]. More recently, studies of allergic diseases have shown that miR-155 plays an indispensible role in the promotion, rather than suppression, of Th2 pathways.
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