MicroRNAs in the key events of systemic lupus erythematosus pathogenesis
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, přehledy
Odkazy
PubMed
27003314
DOI
10.5507/bp.2016.004
Knihovny.cz E-zdroje
- Klíčová slova
- SLE, adaptive immunity, estrogen, genetic predisposition, innate immunity, microRNA,
- MeSH
- adaptivní imunita fyziologie MeSH
- B-lymfocyty imunologie MeSH
- estrogeny fyziologie MeSH
- genetická predispozice k nemoci MeSH
- jednonukleotidový polymorfismus genetika MeSH
- lidé MeSH
- mikro RNA genetika fyziologie MeSH
- modely nemocí na zvířatech MeSH
- myši MeSH
- přirozená imunita fyziologie MeSH
- systémový lupus erythematodes etiologie genetika imunologie MeSH
- T-lymfocyty imunologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- estrogeny MeSH
- mikro RNA 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.