RGD Reference Report - Bone Marrow-Derived Mesenchymal Stem Cells Attenuate Immune-Mediated Liver Injury and Compromise Virus Control During Acute Hepatitis B Virus Infection in Mice.

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Bone Marrow-Derived Mesenchymal Stem Cells Attenuate Immune-Mediated Liver Injury and Compromise Virus Control During Acute Hepatitis B Virus Infection in Mice.
Authors:	Qu, Mengmeng Yuan, Xu Liu, Dan Ma, Yuhong Zhu, Jun Cui, Jun Yu, Mengxue Li, Changyong Guo, Deyin
Citation:	Qu M, etal., Stem Cells Dev. 2017 Jun 1;26(11):818-827. doi: 10.1089/scd.2016.0348. Epub 2017 Feb 2.
RGD ID:	39128174
Pubmed:	PMID:28318408 (View Abstract at PubMed)
DOI:	DOI:10.1089/scd.2016.0348 (Journal Full-text)
Mesenchymal stem cells (MSCs) have been used as therapeutic tools not only for their ability to differentiate toward different cells, but also for their unique immunomodulatory properties. However, it is still unknown how MSCs may affect immunity during hepatitis B virus (HBV) infection. This study was designed to explore the effect of bone marrow-derived MSCs (BM-MSCs) on hepatic natural killer (NK) cells in a mouse model of acute HBV infection. Mice were injected with 1 × 106 BM-MSCs, which stained with chloromethyl derivatives of fluorescein diacetate fluorescent probe, 24 h before hydrodynamic injection of viral DNA (pHBV1.3) through the tail vein. In vivo imaging system revealed that BM-MSCs were accumulated in the injured liver, and they attenuated immune-mediated liver injury during HBV infection, as shown by lower alanine aminotransferase levels, reduced proinflammatory cytokine production, and decreased inflammatory cell infiltration in the liver. Importantly, administration of BM-MSCs restrained the increased expression of natural-killer group 2, member D (NKG2D), an important receptor required for NK cell activation in the liver from HBV-infected mice. BM-MSCs also reduced NKG2D expression on NK cells and suppressed the cytotoxicity of NK cells in vitro. Furthermore, BM-MSC-derived transforming growth factor-β1 suppressed NKG2D expression on NK cells. As a consequence, BM-MSC treatment enhanced HBV gene expression and replication in vivo. These results demonstrate that adoptive transfer of BM-MSCs influences innate immunity and limits immune-mediated liver injury during acute HBV infection by suppressing NK cell activity. Meanwhile, the effect of BM-MSCs on prolonging virus clearance needs to be considered in the future.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
KLRK1	Human	hepatitis B	treatment	ISO	Klrk1 (Mus musculus)		RGD
Klrk1	Rat	hepatitis B	treatment	ISO	Klrk1 (Mus musculus)		RGD
Klrk1	Mouse	hepatitis B	treatment	IEP			RGD

Objects Annotated

Genes (Rattus norvegicus)

Klrk1 (killer cell lectin like receptor K1)

Genes (Mus musculus)

Klrk1 (killer cell lectin-like receptor subfamily K, member 1)

Genes (Homo sapiens)

KLRK1 (killer cell lectin like receptor K1)

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Bone Marrow-Derived Mesenchymal Stem Cells Attenuate Immune-Mediated Liver Injury and Compromise Virus Control During Acute Hepatitis B Virus Infection in Mice.