NDLI: Dicer insufficiency and miR-155 overexpression in lupus Treg cells: an apparent paradox in the setting of an inflammatory milieu1

Content Provider	PubMed Central
Author	Divekar, Anagha A. Dubey, Shweta Gangalum, Pallavi R. Singh, Ram Raj
Abstract	Systemic lupus erythematosus (SLE) is a chroni c autoimmune disease characterized by loss of tolerance to self-antigens and activation of autoreactive T cells. Regulatory T cells (Treg) play a critical role in controlling the activation of autoreactive T cells. Here, we investigated mechanisms of potential Treg defects in SLE using MRL-Faslpr/lpr (MRL/lpr) and MRL-Fas +/+ (MRL+/+) mouse models. We found a significant increase in CD4+CD25+Foxp3+ Treg cells, albeit with an altered phenotype (CD62L–CD69+) and with a reduced suppressive capacity, in the lymphoid organs of MRL strains compared to non-autoimmune C3H mice. A search for mechanisms underlying the altered Treg phenotype in MRL/lpr mice led us to find a profound reduction in Dicer expression and an altered microRNA (miRNA, miR) profile in MRL/lpr Treg cells. Despite having a reduced level of Dicer, MRL/lpr Treg cells exhibited a significant overexpression of several miRNAs including let-7a, let-7f, miR-16, miR-23a, miR-23b, miR-27a and miR-155. Using computational approaches, we identified one of the upregulated miRNAs, miR-155 that can target CD62L and may thus confer the altered Treg phenotype in MRL/lpr mice. In fact, the induced overexpression of miR-155 in otherwise normal (C3H) Treg cells reduced their CD62L expression, which mimics the altered Treg phenotype in MRL/lpr mice. These data suggest a role of Dicer and miR-155 in regulating Treg cell phenotype. Furthermore, simultaneous appearance of Dicer insufficiency and miR-155 overexpression in diseased mice suggests a Dicer-independent alternative mechanism of miRNA regulation under inflammatory conditions.
Related Links	http://dx.doi.org/10.4049/jimmunol.1002218
Ending Page	930
Page Count	7
Starting Page	924
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	2
Volume Number	186
Language	English
Publisher Date	2011-01-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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