MiRNA-Mediated Control of HLA-G Expression and Function

Manaster, Irit; Goldman‐Wohl, Debra; Greenfield, Caryn; Nachmani, Daphna; Tsukerman, Pinchas; Hamani, Yaron; Yagel, Simcha; Mandelboim, Ofer

doi:10.1371/journal.pone.0033395

Cited by 134 publications

(112 citation statements)

References 35 publications

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“…69 In addition, NK cell-mediated cytolysis was increased by overexpression of miR-152 69 and the downregulation of HLA-G-affected LILRB1 (inhibitory receptor) recognition, which resulted in enhanced killing activity of NK cells. 68 These studies further suggest a major role for miR-152 in mediating immune responses. In a more recent study, activated CD4 1 T lymphocytes cultured in the presence or absence of HLA-G were screened for 87 miRNAs and it was found that miR-451 and miR-210 were modulated by soluble HLA-G. 70 The interaction between miR-148 and HLA-C has been reported in studies of HIV infection.…”

Section: Micrornas and Immune Cells At The Maternal-fetal Interfacementioning

confidence: 85%

“…However, it had previously been demonstrated in the context of pregnancy that HLA-G expressed mainly by the extravillous trophoblasts of the placenta could be downregulated by miR-148a and miR-152 by binding to its 39-untranslated region. 68 Similarly miR-152 has been shown to repress HLA-G without affecting the invasiveness of JEG-3 choriocarcinoma cells. 69 In addition, NK cell-mediated cytolysis was increased by overexpression of miR-152 69 and the downregulation of HLA-G-affected LILRB1 (inhibitory receptor) recognition, which resulted in enhanced killing activity of NK cells.…”

Section: Micrornas and Immune Cells At The Maternal-fetal Interfacementioning

confidence: 99%

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MicroRNAs, immune cells and pregnancy

et al. 2014

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MicroRNAs (miRNAs) are a recently discovered class of non-coding RNAs that are expressed in many cell types, where they regulate the expression of complementary RNAs, thus modulating the stability and translation of mRNAs. miRNAs are predicted to regulate the expression of ,50% of all protein coding genes in mammals. Therefore, they participate in virtually all cellular processes investigated so far. Altered miRNAs expressions are associated with both physiological (pregnancy) and pathological processes (cancer). As the dynamic maternal-fetal interface plays a critical role in the maintenance of successful pregnancy, it is not surprising that the miRNAs that are unique to reproductive tissues are abundantly expressed. Research in this field has demonstrated the presence and dysregulation of a distinct set of pregnancy-associated miRNAs; however, most studies have centered on localizing various miRNAs in reproductive microdomains associated with normal or complicated pregnancies. Although several independent miRNA regulatory mechanisms associated with endometrial receptivity, immune cells, angiogenesis and placental development have been studied, miRNA-mediated regulation of pregnancy remains poorly understood. This review provides a summary of the current data on miRNA regulation as well as functional profiles of miRNAs that are found in the uterus, in immune cells associated with maternal tolerance to the fetus, and those involved in angiogenesis and placental development.

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Section: Micrornas and Immune Cells At The Maternal-fetal Interfacementioning

confidence: 85%

Section: Micrornas and Immune Cells At The Maternal-fetal Interfacementioning

confidence: 99%

MicroRNAs, immune cells and pregnancy

et al. 2014

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“…This region consist of 2-7 nucleotides that are perfectly complementary to that of the mRNA. The seed region of miR-148a and miR-148b is the same and the predicted binding energies are similar (Manaster et al, 2012;Tan et al, 2007). Therefore it is thought that these two miRNAs have similar activity.…”

Section: Mir-148a Mir-148b and Mir-152 Expressionmentioning

confidence: 88%

“…These are: miR-148a, miR-148b and miR-152 (Tan et al, 2007). It has been shown that both miR148a and miR-152 can downregulate the expression of HLA-G and reduce the binding of the inhibitory receptor ILT2 to HLA-G cells (Manaster et al, 2012;Zhu et al, 2010). As a consequence, NK cell-mediated cytotoxicity is increased.…”

Section: Micrornasmentioning

confidence: 99%

How Micrornas Affect the Expression of Human Leukocyte Antigeng in Pregnancy

Kempers

Dijk

Oudejans

2012

American Journal of Immunology

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The expression of Human Leukocyte Antigen G (HLA-G) on Fetal Extravillous Trophoblast (EVT) cells during pregnancy plays an important role in preventing the fetus from rejection by suppressing the maternal immune system. Decreased expression levels of HLA-G have already shown to be associated with several complications of pregnancy such as pre-eclampsia. However, it remains largely unknown how HLA-G gene expression is regulated with regard to its function and its complications. Polymorphisms and microRNAs affect HLA-G gene expression and the formation of isoforms. Interestingly, three microRNAs, miR-148a, miR-148b and miR-152, downregulate HLA-G expression with functional consequences. Since HLA-G expression levels are reduced in pre-eclampsia without a known cause, we hypothesize that these microRNAs are involved in the development of pre-eclampsia. This review discusses how microRNAs can affect HLA-G gene expression and its functions. Additionally, the role of microRNAs in the development of pre-eclampsia will be reviewed.

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“…The miRNA regulation of MHC class I has been previously characterized in HLA-C and HLA-G, which are controlled by miR148a and miR-152, respectively (45,46). However, the duck UDA transcript is not a target of either miR-148a or miR-152.…”

Section: Uda Is Regulated By the Let-7 Mirna Familymentioning

confidence: 99%

The Minor MHC Class I Gene UDA of Ducks Is Regulated by Let-7 MicroRNA

Chan

Parks-Dely

Magor

et al. 2016

The Journal of Immunology

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In many nonmammalian vertebrates, the genomic organization of the MHC class I region leads to biased expression of a single classical MHC class I gene coevolving with TAP transporters, whereas class I genes are poorly expressed. This contrasts to the three codominantly expressed classical MHC class I genes in humans and mice. In a sequenced haplotype from White Pekin duck, Anas platyrhynchos, there is one predominantly expressed MHC class I, UAA, although they have five MHC class I genes in the complex, arranged TAP1-TAP2-UAA-UBA-UCA-UDA-UEA. The UAA gene, situated proximal to the TAP2 gene, is expressed at levels 10-fold greater than that of another expressed gene, UDA. Three duck MHC class I genes (UBA, UCA, and UEA) are predicted to be partially or completely inactivated by promoter defects, introduction of in-frame stop codon, or the lack of a polyadenylation signal. In this study, we confirm that UBA, UCA, and UEA are indeed inactivated through genetic defects at the promoter, whereas UAA and UDA have functionally equivalent promoters. To examine promoter accessibility, we performed bisulfite sequencing and show that none of the MHC class I promoters are inactivated by methylation. We determine that UDA is differentially regulated through its 3′ untranslated region. Namely, expression of UDA is downregulated by let-7 microRNA, whereas the predominantly expressed MHC class I UAA is not. Regulation of UDA by let-7 microRNA suggests that the lower expression level is maintained for its function in immunity.

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MiRNA-Mediated Control of HLA-G Expression and Function

Cited by 134 publications

References 35 publications

MicroRNAs, immune cells and pregnancy

MicroRNAs, immune cells and pregnancy

How Micrornas Affect the Expression of Human Leukocyte Antigeng in Pregnancy

The Minor MHC Class I Gene UDA of Ducks Is Regulated by Let-7 MicroRNA

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