کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2170608 1093390 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Role of microRNA-155 in autoimmunity
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Role of microRNA-155 in autoimmunity
چکیده انگلیسی

MicroRNAs (miRNAs) have recently emerged as a major class of gene expression regulators linked to most biological functions. MiR-155 is encoded within a region known as B cell integration cluster (Bic) gene, identified originally as a frequent integration site for the avian leukosis virus. Disregulation of endogenous miR-155 has been implicated in the pathogenesis of human cancers. Recently, aberrant expression of miR-155 was observed in many autoimmune conditions, including rheumatoid arthritis (RA), multiple sclerosis (MS), and systemic lupus erythematosus (SLE). Moreover, functional analysis demonstrated that miR-155 has powerful regulatory potential in a wide variety of immune cells through targeting specific mRNAs. Since pathogenic immune cells play a pivotal role in pathogenesis of human autoimmune diseases, miR-155 might be a versatile therapeutic target. This review will discuss the current understandings for the role of miR-155 in autoimmunity.


► MiR-155 has powerful regulatory potential in a wide variety of immune cells through targeting specific mRNAs.
► Aberrant expression of miR-155 has been observed in many human autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.
► MiR-155 deficiency can prevent development of autoimmunity in animal models.
► Expression level of miR-155 could be effectively regulated by targeting specific signaling molecules.
► Since disregulated expression of miR-155 is associated with increased risk of cancer, an appropriate level of miR-155 may be important for maintaining normal immune responses.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine & Growth Factor Reviews - Volume 22, Issue 3, June 2011, Pages 141–147
نویسندگان
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