Abstract
MicroRNAs (miRNAs) are small noncoding conserved RNAs containing 19 to 24 nucleotides that are regulators of post-translational modifications and are involved in the majority of biological processes such as immune homeostasis, T helper cell differentiation, central and peripheral tolerance, and immune cell development. Autoimmune diseases are characterized by immune system dysregulation, which ultimately leads to destructive responses to self-antigens. A large body of literature suggests that autoimmune diseases and immune dysregulation are associated with different miRNA expression changes in the target cells and tissues of adaptive or innate immunity. miR-155 is identified as a critical modulator of immune responses. Recently conducted studies on the expression profile of miR-155 suggest that the altered expression and function of miR-155 can mediate vulnerability to autoimmune diseases and cause significant dysfunction of the immune system.
Highlights
Understanding miRNAs’ role opened a new aspect of discovering disease pathogenesis and conferred a targeted therapy for a diverse spectrum of diseases. miRNAs are small noncoding conserved RNAs, with a length of 19 to 24 nucleotides and regulators of post-translational modifications [1, 2]
We suggest that treatment with several popular drugs would decrease the expression of miR-155, which could be considered as a target for multiple sclerosis (MS) therapy
The present review was conducted to discuss the available data associated with miR-155 expression and function alterations in the immune system from human autoimmune disease as well as related animal models. miR-155 exerts a significant impact on the homeostasis and development of the immune system
Summary
Understanding miRNAs’ role opened a new aspect of discovering disease pathogenesis and conferred a targeted therapy for a diverse spectrum of diseases. miRNAs are small noncoding conserved RNAs, with a length of 19 to 24 nucleotides and regulators of post-translational modifications [1, 2]. Lack of miR-155 results in Othe overexpression of Peli in CD4+ T cells, which decreased the accumulation of c-Rel consecutively This process led to the compromised expression of CD40L on CD4+ T cells and impaired proliferation of antigen-specific CD4+ T cells at the late TFH cell differentiation stage [24]. Mature DCs from miR-155 deficient mice exhibited functional and phenotypic defects These defects in DCs are such as typical DCs morphology, decreased in the upregulation of costimulatory molecules, especially CD40 and CD86, robust decreased ability for antigen-specific CD4+ T cell activation and proliferation [17]. During human Mo-DC and several subtypes of mice DC activation and maturation, the miR-155 expression level is increased; the c-Fos mRNA level is downregulated. Alteration of miR-155 was detected in human and animal models of various autoimmune diseases, including rheumatoid arthritis (RA), multiple sclerosis (MS), systemic sclerosis (SSc), systemic lupus erythematosus (SLE), and so on
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