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- W4322095724 abstract "Abstract SLE is a heterogeneous autoimmune disease and the specific cause remains unknown. B and T cell abnormalities are considered to play a central role in SLE. More recently, microRNAs (miRNAs), a group of small (~22nt) non-coding RNAs have been studied in SLE patients. miR16, targeting Bcl-2, regulates cell apoptosis.miR-146a, which plays a role in downregulation of type I interferon signaling, is found to be decreased in SLE. In NZB/W F1 mouse lupus model, these two particular microRNAs will be investigated in order to identify the microRNAs in regulation of balancing of B and T cell immunity. In preliminary studies, we treated B/W mice with IFNα or IFNλ for 12 week period and IFNα treated group, but not the IFNλ group developed much earlier and more severe lupus-disease than others. We found that spleen cells from IFNα or IFNλ treated B/W mice had similar level of miR16 and miR146a with control B/W, and all the B/W mice showed a pronounced underexpression of these two miRs comparing to C57 mice. By flow cytometry, only IFNα treated group cells showed hyper-activation of B and T cells, and decreased regulatory B. Thus, it is likely that due to the failure to turn off activation of type I interferon signaling in B/W mice by miR146a and anti-apoptotic effects in activated B cells resulting from low level miR16 may drive the acceleration of lupus-disease in the lupus-prone B/W mice." @default.
- W4322095724 created "2023-02-26" @default.
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- W4322095724 date "2010-04-01" @default.
- W4322095724 modified "2023-09-30" @default.
- W4322095724 title "MicroRNAs (miR16 and miR146a) regulation of lupus development in NZB/W F1 mouse model (87.9)" @default.
- W4322095724 doi "https://doi.org/10.4049/jimmunol.184.supp.87.9" @default.
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