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Article ; Online: Pathogenic Role of Type I Interferons in HIV-Induced Immune Impairments in Humanized Mice.

Su, Lishan

2019 Volume 16, Issue 3, Page(s) 224–229

Abstract: Purpose of review: Recent findings on the critical pathogenic role of type 1 interferons (IFN-I) in HIV-1 persistence in humanized mice suggest that inhibiting IFN-I signaling transiently will reverse HIV-induced inflammatory diseases and rescue anti- ... ...

Abstract	Purpose of review: Recent findings on the critical pathogenic role of type 1 interferons (IFN-I) in HIV-1 persistence in humanized mice suggest that inhibiting IFN-I signaling transiently will reverse HIV-induced inflammatory diseases and rescue anti-HIV immunity to control HIV-1 reservoirs. Recent findings: In both humanized mice and in monkeys, IFN-I signaling is functionally defined to play an important role in suppressing early HIV-1 and SIV infection. During persistent infection in humanized mice, however, IFN-I signaling is revealed to induce T cell depletion and impairment. Interestingly, in HIV-infected mice with effective combination antiretroviral therapy (cART), blocking IFN-I signaling reverses HIV-induced inflammation, rescues anti-HIV T cells, and reduces HIV-1 reservoirs. These findings functionally define the role of IFN-I in HIV-1 reservoir persistence and suggest that blocking IFN-I signaling will provide a novel therapeutic strategy to (i) reverse inflammation-associated diseases in HIV patients under cART, (ii) rescue host anti-HIV immunity, and (iii) reduce or control HIV-1 reservoirs.
MeSH term(s)	Animals ; Anti-Retroviral Agents/therapeutic use ; HIV Infections/drug therapy ; HIV Infections/pathology ; HIV-1/immunology ; Humans ; Interferon Type I/metabolism ; Mice ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Chemical Substances	Anti-Retroviral Agents ; Interferon Type I
Language	English
Publishing date	2019-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2151206-1
ISSN	1548-3576 ; 1548-3568
ISSN (online)	1548-3576
ISSN	1548-3568
DOI	10.1007/s11904-019-00444-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Disruption of HBx-DDB1 by NTZ: New Mechanistic Insight Into an Old Drug With Broad Anti-infective Activities.

Su, Lishan

Cellular and molecular gastroenterology and hepatology

2018 Volume 7, Issue 2, Page(s) 289–290

MeSH term(s)	Hepatitis B virus/genetics ; Thiazoles
Chemical Substances	Thiazoles ; nitazoxanide (SOA12P041N)
Language	English
Publishing date	2018-11-15
Publishing country	United States
Document type	Editorial ; Comment
ISSN	2352-345X
ISSN (online)	2352-345X
DOI	10.1016/j.jcmgh.2018.10.013
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A pathogenic role of plasmacytoid dendritic cells in autoimmunity and chronic viral infection.

Barrat, Franck J / Su, Lishan

The Journal of experimental medicine

2019 Volume 216, Issue 9, Page(s) 1974–1985

Abstract: Following the discovery of plasmacytoid dendritic cells (pDCs) and of their extraordinary ability to produce type I IFNs (IFN-I) in response to TLR7 and TLR9 stimulation, it is assumed that their main function is to participate in the antiviral response. ...

Abstract	Following the discovery of plasmacytoid dendritic cells (pDCs) and of their extraordinary ability to produce type I IFNs (IFN-I) in response to TLR7 and TLR9 stimulation, it is assumed that their main function is to participate in the antiviral response. There is increasing evidence suggesting that pDCs and/or IFN-I can also have a detrimental role in a number of inflammatory and autoimmune diseases, in the context of chronic viral infections and in cancers. Whether these cells should be targeted in patients and how much of their biology is connected to IFN-I production remains unclear and is discussed here.
MeSH term(s)	Animals ; Autoimmunity ; Chronic Disease ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Immunity, Innate ; Models, Biological ; Virus Diseases/immunology ; Virus Diseases/therapy
Language	English
Publishing date	2019-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20181359
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Article ; Online: Phenotypic and Functional Study of Human Plasmacytoid Dendritic Cells.

Li, Guangming / Cheng, Liang / Su, Lishan

Current protocols

2021 Volume 1, Issue 4, Page(s) e50

Abstract: Plasmacytoid dendritic cells (pDCs) are a distinct lineage of bone-marrow-derived cells that reside mainly in blood and lymphoid organs in the steady state but are also present in sites of infection, inflammation, and cancer. The protocols in this ... ...

Abstract	Plasmacytoid dendritic cells (pDCs) are a distinct lineage of bone-marrow-derived cells that reside mainly in blood and lymphoid organs in the steady state but are also present in sites of infection, inflammation, and cancer. The protocols in this article describes (1) detection and quantification of human pDCs in peripheral blood; (2) isolation of human pDCs by magnetic-activated cell sorting (MACS) and fluorescence-activated cell sorting (FACS); (3) evaluation of human pDC function by stimulation with TLR7 or TLR9 agonists; (4) detection of human pDCs in lymphoid tissues of humanized mice (hu-mice) by flow cytometry; (5) functional study of human pDC in hu-mice in vivo; and (6) specific depletion of human pDCs in vivo in hu-mice using monoclonal antibody targeting human pDCs. These assays thus provide comprehensive methods for phenotypic and functional studies in vitro and for the investigation of human plasmacytoid dendritic cells in hu-mice in vivo. © 2021 Wiley Periodicals LLC. Basic Protocol 1: Analysis of pDCs in human peripheral blood mononuclear cells Basic Protocol 2: pDC separation using MACS beads Alternate Protocol 1: pDC sorting using flow cytometer Basic Protocol 3: Evaluation of human pDC function by stimulation with TLR agonists in vitro Alternate Protocol 2: Intracellular staining of cytokines in pDCs Basic Protocol 4: Phenotypic analysis of human pDCs from lymphoid organs in humanized mice Basic Protocol 5: Functional study of human pDCs in humanized mice during HIV infection Basic Protocol 6: pDC depletion and assessment of pDC depletion in acute HIV-infected in humanized mice.
MeSH term(s)	Animals ; Dendritic Cells ; Flow Cytometry ; HIV Infections ; Humans ; Leukocytes, Mononuclear ; Mice
Language	English
Publishing date	2021-04-08
Publishing country	United States
Document type	Journal Article
ISSN	2691-1299
ISSN (online)	2691-1299
DOI	10.1002/cpz1.50
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Article ; Online: Vpr Enhances HIV-1 Env Processing and Virion Infectivity in Macrophages by Modulating TET2-Dependent IFITM3 Expression.

Wang, Qi / Su, Lishan

mBio

2019 Volume 10, Issue 4

Abstract: HIV-1 Vpr enhances viral replication in human macrophages via multiple mechanisms that are not clearly defined. It does not affect HIV-1 virion production during the first round of infection. We have recently discovered that Vpr targets the DNA ... ...

Abstract	HIV-1 Vpr enhances viral replication in human macrophages via multiple mechanisms that are not clearly defined. It does not affect HIV-1 virion production during the first round of infection. We have recently discovered that Vpr targets the DNA demethylase TET2 for degradation, which leads to sustained interleukin-6 (IL-6) expression and elevated HIV-1 replication. We report here that Vpr enhanced Env processing in infected macrophages, associated with increased Env incorporation into virions with higher infectivity. Interestingly, IFITM3 was constitutively expressed in macrophages in a TET2-dependent fashion. We showed that Vpr-enhanced Env processing depended genetically on TET2 and IFITM3. We further showed that Vpr reduced IFITM3 expression by reducing demethylation of the IFITM3 promoter in macrophages, associated with degradation of TET2 and reduced TET2 binding to the IFITIM3 promoter. Our findings indicate that the Vpr-TET2 axis enhances HIV-1 replication in macrophages via two independent mechanisms: reduced IFTIM3 expression to enhance Env processing and virion infectivity and sustained IL-6 expression to increase HIV-1 replication. The Vpr-TET2 axis may provide a novel target to develop therapeutics to inhibit HIV-1 infection and pathogenesis.
MeSH term(s)	Anti-HIV Agents/pharmacology ; Carrier Proteins ; Cell Line ; DNA Demethylation ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Dioxygenases ; Gene Expression Regulation, Viral ; HIV-1/drug effects ; HIV-1/genetics ; HIV-1/metabolism ; HIV-1/pathogenicity ; Humans ; Interleukin-6/metabolism ; Macrophages/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Virion/genetics ; Virion/pathogenicity ; Virus Replication/physiology ; env Gene Products, Human Immunodeficiency Virus/metabolism ; vpr Gene Products, Human Immunodeficiency Virus/genetics ; vpr Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	Anti-HIV Agents ; Carrier Proteins ; DNA-Binding Proteins ; IFITM3 protein, human ; Interleukin-6 ; Membrane Proteins ; Proto-Oncogene Proteins ; RNA-Binding Proteins ; env Gene Products, Human Immunodeficiency Virus ; vpr Gene Products, Human Immunodeficiency Virus ; Dioxygenases (EC 1.13.11.-) ; TET2 protein, human (EC 1.13.11.-)
Language	English
Publishing date	2019-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.01344-19
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Article ; Online: Generation and characterization of mature hepatocyte organoids for liver metabolic studies.

Liu, Yuchen / Zhou, Yaxing / Ahodantin, James / Jin, Yu / Zhu, Juanjuan / Sun, Zhonghe / Wu, Xiaolin / Su, Lishan / Yang, Yingzi

Journal of cell science

2024

Abstract: Hepatocyte organoids (HOs) generated in vitro recently are powerful tools for liver regeneration. However, the reported HOs were mostly fetal in nature with low expression levels of metabolic genes characteristic of adult liver functions, hampering their ...

Abstract	Hepatocyte organoids (HOs) generated in vitro recently are powerful tools for liver regeneration. However, the reported HOs were mostly fetal in nature with low expression levels of metabolic genes characteristic of adult liver functions, hampering their application in studying metabolic regulations and therapeutic testing for liver disorders. We report development of novel culture conditions that contains optimized levels of Triiodothyronine (T3) with the removal of growth factors, enabled successful generation of mature hepatocyte organoids (MHOs) with metabolic functions characteristic of adult livers of both mouse and human origins. We showed that the MHOs can be used to study various metabolic functions including bile and urea production, zonal metabolic gene expression, and metabolic alterations in both alcoholic and non-alcoholic fatty liver diseases as well hepatocyte proliferation, injury, and cell fate changes. Notably, the MHOs derived from human fetal hepatoblasts also showed improved hepatitis B virus (HBV) infection. Therefore, these MHOs provide a powerful in vitro model for studies of human liver physiology and diseases. The human MHOs are potentially a robust research tools for therapeutic development as well.
Language	English
Publishing date	2024-05-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.261961
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Article ; Online: Studying human immunology and immunopathology in humanized mice transplanted with human lymphoid tissues and immune cells.

Su, Lishan

Cellular & molecular immunology

2012 Volume 9, Issue 3, Page(s) 191–192

MeSH term(s)	Animals ; Animals, Inbred Strains ; Disease Models, Animal ; Graft Rejection/etiology ; Graft Rejection/immunology ; Humans ; Immune System/cytology ; Immune System Diseases/genetics ; Immune System Diseases/immunology ; Lymphoid Tissue/immunology ; Mice ; Mice, SCID ; Organ Transplantation ; Research
Language	English
Publishing date	2012-05-07
Publishing country	China
Document type	Editorial
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/cmi.2012.4
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Article: CTLA-4 antibody-drug conjugate reveals autologous destruction of B-lymphocytes associated with regulatory T cell impairment.

Muthana, Musleh M / Du, Xuexiang / Liu, Mingyue / Wang, Xu / Wu, Wei / Ai, Chunxia / Su, Lishan / Zheng, Pan / Liu, Yang

bioRxiv : the preprint server for biology

2023

Abstract: Germline CTLA-4 deficiency causes severe autoimmune diseases characterized by dysregulation of ... ...

Abstract	Germline CTLA-4 deficiency causes severe autoimmune diseases characterized by dysregulation of Foxp3
Language	English
Publishing date	2023-08-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.01.530608
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Article ; Online: CTLA-4 antibody-drug conjugate reveals autologous destruction of B-lymphocytes associated with regulatory T cell impairment.

Muthana, Musleh M / Du, Xuexiang / Liu, Mingyue / Wang, Xu / Wu, Wei / Ai, Chunxia / Su, Lishan / Zheng, Pan / Liu, Yang

eLife

2023 Volume 12

Abstract: Germline CTLA-4 deficiency causes severe autoimmune diseases characterized by dysregulation of ... ...

Abstract	Germline CTLA-4 deficiency causes severe autoimmune diseases characterized by dysregulation of Foxp3
MeSH term(s)	B-Lymphocytes/drug effects ; B-Lymphocytes/immunology ; Abatacept/pharmacology ; Animals ; Mice ; CTLA-4 Antigen/genetics ; CTLA-4 Antigen/immunology ; Lymphocyte Depletion ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Apoptosis/drug effects ; Immunoglobulins/blood ; Immunoglobulins/immunology ; CHO Cells ; Cricetulus ; Mice, Inbred C57BL ; Male ; Female
Chemical Substances	Abatacept (7D0YB67S97) ; CTLA-4 Antigen ; Immunoglobulins
Language	English
Publishing date	2023-12-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.87281
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Review of Lambda Interferons in Hepatitis B Virus Infection: Outcomes and Therapeutic Strategies

Novotny, Laura A. / Evans, John Grayson / Su, Lishan / Guo, Haitao / Meissner, Eric G.

Viruses. 2021 June 09, v. 13, no. 6

2021

Abstract: Hepatitis B virus (HBV) chronically infects over 250 million people worldwide and causes nearly 1 million deaths per year due to cirrhosis and liver cancer. Approved treatments for chronic infection include injectable type-I interferons and nucleos(t)ide ...

Abstract	Hepatitis B virus (HBV) chronically infects over 250 million people worldwide and causes nearly 1 million deaths per year due to cirrhosis and liver cancer. Approved treatments for chronic infection include injectable type-I interferons and nucleos(t)ide reverse transcriptase inhibitors. A small minority of patients achieve seroclearance after treatment with type-I interferons, defined as sustained absence of detectable HBV DNA and surface antigen (HBsAg) antigenemia. However, type-I interferons cause significant side effects, are costly, must be administered for months, and most patients have viral rebound or non-response. Nucleos(t)ide reverse transcriptase inhibitors reduce HBV viral load and improve liver-related outcomes, but do not lower HBsAg levels or impart seroclearance. Thus, new therapeutics are urgently needed. Lambda interferons (IFNLs) have been tested as an alternative strategy to stimulate host antiviral pathways to treat HBV infection. IFNLs comprise an evolutionarily conserved innate immune pathway and have cell-type specific activity on hepatocytes, other epithelial cells found at mucosal surfaces, and some immune cells due to restricted cellular expression of the IFNL receptor. This article will review work that examined expression of IFNLs during acute and chronic HBV infection, the impact of IFNLs on HBV replication in vitro and in vivo, the association of polymorphisms in IFNL genes with clinical outcomes, and the therapeutic evaluation of IFNLs for the treatment of chronic HBV infection.
Keywords	DNA ; Hepatitis B virus ; RNA-directed DNA polymerase ; hepatitis B ; hepatocytes ; liver neoplasms ; surface antigens ; therapeutics ; viral load
Language	English
Dates of publication	2021-0609
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v13061090
Database	NAL-Catalogue (AGRICOLA)

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