Abstract
Systemic lupus erythematosus (SLE) is an archetype autoimmune disease characterized by a myriad of immunoregulatory abnormalities that drives injury to multiple tissues and organs. Due to the involvement of various immune cells, inflammatory cytokines, and related signaling pathways, researchers have spent a great deal of effort to clarify the complex etiology and pathogenesis of SLE. Nevertheless, current understanding of the pathogenesis of SLE is still in the early stages, and available nonspecific treatment options for SLE patients remain unsatisfactory. First discovered in 1993, microRNAs (miRNAs) are small RNA molecules that control the expression of 1/3 of human genes at the post-transcriptional level and play various roles in gene regulation. The aberrant expression of miRNAs in SLE patients has been intensively studied, and further studies have suggested that these miRNAs may be potentially relevant to abnormal immune responses and disease progression in SLE. The aim of this review was to summarize the specific miRNAs that have been observed aberrantly expressed in several important pathogenetic processes in SLE, such as DCs abnormalities, overactivation and autoantibody production of B cells, aberrant activation of CD4+ T cells, breakdown of immune tolerance, and abnormally increased production of inflammatory cytokines. Our summary highlights a novel perspective on the intricate regulatory network of SLE, which helps to enrich our understanding of this disorder and ignite future interest in evaluating the molecular regulation of miRNAs in autoimmunity SLE.
Highlights
Systemic lupus erythematosus (SLE) is a severe autoimmune inflammatory disease with a broad range of clinical manifestations characterized by loss of tolerance to selfantigens, activation of dysregulated autoreactive T cells and B cells, production of autoantibodies and perturbed cytokine activities [1]
MiR-148a directly inhibits DNMT1 expression by targeting the protein coding region of the transcript. These data clearly showed that abnormally expressed miRNAs in SLE patients had a critical functional link with the aberrant DNA hypomethylation in lupus CD4+ T cells, resulting in the overexpression of autoimmune-associated methylationsensitive genes, such as those that encode CD70 (tumor necrosis factor superfamily, member 7 [TNFSF7]), CD40 ligand (TNFSF5), and lymphocyte function-associated antigen 1 (LAF-1, integrin aLb2, CD11a/CD18) [54], which contributed to the autoreactivity and overstimulation of CD4+ T cells in SLE [51]
SLE is a heterogeneous chronic inflammatory autoimmune disorder, which is characterized by aberrant activation of lymphocytes, auto-antibodies, and inflammatory cytokine production [1]
Summary
The aberrant expression of miRNAs in SLE patients has been intensively studied, and further studies have suggested that these miRNAs may be potentially relevant to abnormal immune responses and disease progression in SLE. The aim of this review was to summarize the specific miRNAs that have been observed aberrantly expressed in several important pathogenetic processes in SLE, such as DCs abnormalities, overactivation and autoantibody production of B cells, aberrant activation of CD4+ T cells, breakdown of immune tolerance, and abnormally increased production of inflammatory cytokines. Our summary highlights a novel perspective on the intricate regulatory network of SLE, which helps to enrich our understanding of this disorder and ignite future interest in evaluating the molecular regulation of miRNAs in autoimmunity SLE
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