Deletion of microRNA-155 reduces autoantibody responses and alleviates lupus-like disease in the Fas mouse
Proceedings of the National Academy of Sciences of the United States of America, ISSN: 0027-8424, Vol: 110, Issue: 50, Page: 20194-20199
2013
- 89Citations
- 59Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations89
- Citation Indexes89
- 89
- CrossRef77
- Captures59
- Readers59
- 59
Article Description
MicroRNA-155 (miR-155) regulates antibody responses and subsequent B-cell effector functions to exogenous antigens. However, the role of miR-155 in systemic autoimmunity is not known. Using the death receptor deficient (Fas ) lupus-prone mouse, we show here that ablation of miR-155 reduced autoantibody responses accompanied by a decrease in serum IgG but not IgM anti-dsDNA antibodies and a reduction of kidney inflammation. MiR-155 deletion in Fas B cells restored the reduced SH2 domain-containing inositol 5′-phosphatase 1 to normal levels. In addition, coaggregation of the Fc γ receptor IIB with the B-cell receptor in miR-155-Fas B cells resulted in decreased ERK activation, proliferation, and production of switched antibodies compared with miR-155 sufficient Fas B cells. Thus, by controlling the levels of SH2 domain-containing inositol 5′-phosphatase 1, miR-155 in part maintains an activation threshold that allows B cells to respond to antigens.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84890284251&origin=inward; http://dx.doi.org/10.1073/pnas.1317632110; http://www.ncbi.nlm.nih.gov/pubmed/24282294; https://pnas.org/doi/full/10.1073/pnas.1317632110; https://dx.doi.org/10.1073/pnas.1317632110; https://www.pnas.org/content/110/50/20194; http://www.pnas.org/lookup/doi/10.1073/pnas.1317632110; http://www.pnas.org/content/110/50/20194; http://www.pnas.org/content/110/50/20194.abstract; http://www.pnas.org/content/110/50/20194.full.pdf; https://www.pnas.org/content/110/50/20194.abstract; https://www.pnas.org/content/pnas/110/50/20194.full.pdf; http://www.pnas.org/cgi/doi/10.1073/pnas.1317632110; http://f1000.com/prime/718187650#eval793487736
Proceedings of the National Academy of Sciences
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