MicroRNAs in the key events of systemic lupus erythematosus pathogenesis
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Review
PubMed
27003314
DOI
10.5507/bp.2016.004
Knihovny.cz E-resources
- Keywords
- SLE, adaptive immunity, estrogen, genetic predisposition, innate immunity, microRNA,
- MeSH
- Adaptive Immunity physiology MeSH
- B-Lymphocytes immunology MeSH
- Estrogens physiology MeSH
- Genetic Predisposition to Disease MeSH
- Polymorphism, Single Nucleotide genetics MeSH
- Humans MeSH
- MicroRNAs genetics physiology MeSH
- Disease Models, Animal MeSH
- Mice MeSH
- Immunity, Innate physiology MeSH
- Lupus Erythematosus, Systemic etiology genetics immunology MeSH
- T-Lymphocytes immunology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Estrogens MeSH
- MicroRNAs MeSH
BACKGROUND: Small non-coding RNA molecules (miRs) are involved in immune cell maturation and function and might influence immunopathological processes of systemic lupus erythematosus (SLE) pathogenesis. METHODS AND RESULTS: This paper presents the results of a literature search for publications dealing with the relationship between miRs and pathological factors related to SLE such as genetic background, immune dysregulation and gender-associated differences participating in SLE development. In SLE, distinct miRs are differentially expressed in SLE cells of innate and adaptive immunity. The miR-146a and miR-155 genes, among others, interfere with intracellular signalling pathways downstream of toll-like receptors 7 and 9 (TLR- 7, TLR-9) and influences interferon (IFN)-type I synthesis in plasmacytoid dendritic cells. In T and B cells, miR-126, miR-21, miR-146a, miR-155, miR-1246 and others might influence gene expression by epigenetic modifications, support abnormal cytosine release, differentiation of cell subsets, B cell hyperactivity and autoantibody production. Besides, estrogen might up- and downregulate immunologically active miRs, which are potential mediators of hormonal influences in SLE development. Moreover, SLE genetic basis included some polymorphisms of the miR-146a gene, which varies across populations. CONCLUSION: Distinct miRs are differentially expressed in both SLE mice models and human patients and promote autoimmune features of immune processes. MiRs are important molecules modulating susceptibility to SLE as well as its onset, clinical diversity and progression.
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