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n2:pmcid: PMC0
bibo:doi: 10.1371%2Fjournal.ppat.1004032
n5:contains: _:vb29675264 _:vb29675286 _:vb29675246 _:vb29675204

Subject Item: _:vb29675204
rdf:type: n5:Section
dc:title: introduction
n5:contains: _:vb29675236 _:vb29675237 _:vb29675238 _:vb29675239 _:vb29675232 _:vb29675233 _:vb29675234 _:vb29675235 _:vb29675244 _:vb29675245 _:vb29675240 _:vb29675241 _:vb29675242 _:vb29675243 _:vb29675220 _:vb29675221 _:vb29675222 _:vb29675223 _:vb29675216 _:vb29675217 _:vb29675218 _:vb29675219 _:vb29675228 _:vb29675229 _:vb29675230 _:vb29675231 _:vb29675224 _:vb29675225 _:vb29675226 _:vb29675227 _:vb29675205 _:vb29675206 _:vb29675207 _:vb29675212 _:vb29675213 _:vb29675214 _:vb29675215 _:vb29675208 _:vb29675209 _:vb29675210 _:vb29675211

Subject Item: _:vb29675205
rdf:type: n2:Context
rdf:value: Chronic hepatitis B virus (HBV) infection results in liver fibrosis/cirrhosis and development of hepatocellular carcinoma (HCC) [>>1<<], [2]. Establishment of chronic HBV infection is inversely associated with patient's age with neonatal and infants most susceptible, while adults are mostly resistant to chronic infection [3], [4].
n2:mentions: n3:21705499

Subject Item: _:vb29675206
rdf:type: n2:Context
rdf:value: Chronic hepatitis B virus (HBV) infection results in liver fibrosis/cirrhosis and development of hepatocellular carcinoma (HCC) [1], [>>2<<]. Establishment of chronic HBV infection is inversely associated with patient's age with neonatal and infants most susceptible, while adults are mostly resistant to chronic infection [3], [4].
n2:mentions: n3:22105184

Subject Item: _:vb29675207
rdf:type: n2:Context
rdf:value: Establishment of chronic HBV infection is inversely associated with patient's age with neonatal and infants most susceptible, while adults are mostly resistant to chronic infection [3], [>>4<<]. Chronic HBV infection is associated with impaired immune responses to viral antigens and chronic inflammation in the liver, leading to progressive liver diseases. Though HBV-induced liver disease is predominately a chronic disease,
n2:mentions: n3:19840256

Subject Item: _:vb29675208
rdf:type: n2:Context
rdf:value: Though HBV-induced liver disease is predominately a chronic disease, requiring decades of chronic infection and liver inflammation [>>5<<], [6], [7], HBV infection occasionally results in accelerated liver disease and liver failure during acute infection [8], [9].
n2:mentions: n3:17520515

Subject Item: _:vb29675209
rdf:type: n2:Context
rdf:value: Though HBV-induced liver disease is predominately a chronic disease, requiring decades of chronic infection and liver inflammation [5], [>>6<<], [7], HBV infection occasionally results in accelerated liver disease and liver failure during acute infection [8], [9].
n2:mentions: n3:22171125

Subject Item: _:vb29675210
rdf:type: n2:Context
rdf:value: Though HBV-induced liver disease is predominately a chronic disease, requiring decades of chronic infection and liver inflammation [5], [6], [>>7<<], HBV infection occasionally results in accelerated liver disease and liver failure during acute infection [8], [9].
n2:mentions: n3:17570208

Subject Item: _:vb29675211
rdf:type: n2:Context
rdf:value: liver disease is predominately a chronic disease, requiring decades of chronic infection and liver inflammation [5], [6], [7], HBV infection occasionally results in accelerated liver disease and liver failure during acute infection [>>8<<], [9]. The development of preventive vaccines and therapeutics using chimpanzees and surrogate hepatitis virus-small animal models has played a significant role in preventing new infections and controlling HBV-induced liver diseases.
n2:mentions: n3:23185381

Subject Item: _:vb29675212
rdf:type: n2:Context
rdf:value: disease is predominately a chronic disease, requiring decades of chronic infection and liver inflammation [5], [6], [7], HBV infection occasionally results in accelerated liver disease and liver failure during acute infection [8], [>>9<<]. The development of preventive vaccines and therapeutics using chimpanzees and surrogate hepatitis virus-small animal models has played a significant role in preventing new infections and controlling HBV-induced liver diseases.
n2:mentions: n3:20421498

Subject Item: _:vb29675213
rdf:type: n2:Context
rdf:value: However, HBV is endemic in many developing countries with over 350 million people worldwide chronically infected [>>10<<]. Delineation of the mechanisms by which HBV evades host immunity to establish chronic infection and promote liver disease is hampered by the lack of robust animal models [11], [12], [13].
n2:mentions: n3:22898798

Subject Item: _:vb29675214
rdf:type: n2:Context
rdf:value: Delineation of the mechanisms by which HBV evades host immunity to establish chronic infection and promote liver disease is hampered by the lack of robust animal models [>>11<<], [12], [13].
n2:mentions: n3:21718641

Subject Item: _:vb29675215
rdf:type: n2:Context
rdf:value: Delineation of the mechanisms by which HBV evades host immunity to establish chronic infection and promote liver disease is hampered by the lack of robust animal models [11], [>>12<<], [13].
n2:mentions: n3:20179350

Subject Item: _:vb29675216
rdf:type: n2:Context
rdf:value: Delineation of the mechanisms by which HBV evades host immunity to establish chronic infection and promote liver disease is hampered by the lack of robust animal models [11], [12], [>>13<<].
n2:mentions: n3:22162746

Subject Item: _:vb29675217
rdf:type: n2:Context
rdf:value: To overcome host species restriction barrier for in vivo infection and disease modeling, several human-murine chimeric liver models have been developed [>>14<<]. The Alb-uPA/SCID humanized mouse with high human adult hepatocyte repopulation can be infected with HCV/HBV [14]. Additionally, the fumarylacetoacetate hydrolase (Fah)-Rag2-γC-null mice also allow human hepatocytes engraftment and HCV
n2:mentions: n3:11479625

Subject Item: _:vb29675218
rdf:type: n2:Context
rdf:value: The Alb-uPA/SCID humanized mouse with high human adult hepatocyte repopulation can be infected with HCV/HBV [>>14<<]. Additionally, the fumarylacetoacetate hydrolase (Fah)-Rag2-γC-null mice also allow human hepatocytes engraftment and HCV infection [15], [16], [17]. However, these human-murine chimeric liver models lack a functional human immune system,
n2:mentions: n3:11479625

Subject Item: _:vb29675219
rdf:type: n2:Context
rdf:value: Additionally, the fumarylacetoacetate hydrolase (Fah)-Rag2-γC-null mice also allow human hepatocytes engraftment and HCV infection [>>15<<], [16], [17].
n2:mentions: n3:17664939

Subject Item: _:vb29675220
rdf:type: n2:Context
rdf:value: Additionally, the fumarylacetoacetate hydrolase (Fah)-Rag2-γC-null mice also allow human hepatocytes engraftment and HCV infection [15], [>>16<<], [17]. However, these human-murine chimeric liver models lack a functional human immune system, thus it is not possible to study host immune response and hepatitis virus-induced immunopathology [14], [17]. To overcome the limitations
n2:mentions: n3:18077355

Subject Item: _:vb29675221
rdf:type: n2:Context
rdf:value: Additionally, the fumarylacetoacetate hydrolase (Fah)-Rag2-γC-null mice also allow human hepatocytes engraftment and HCV infection [15], [16], [>>17<<]. However, these human-murine chimeric liver models lack a functional human immune system, thus it is not possible to study host immune response and hepatitis virus-induced immunopathology [14], [17]. To overcome the limitations associated
n2:mentions: n3:20179355

Subject Item: _:vb29675222
rdf:type: n2:Context
rdf:value: However, these human-murine chimeric liver models lack a functional human immune system, thus it is not possible to study host immune response and hepatitis virus-induced immunopathology [>>14<<], [17]. To overcome the limitations associated with current chimeric human-murine liver mouse models, we have recently developed a humanized mouse model with both human immune system and liver cells (AFC8-hu HSC/Hep mice) [18], [19].
n2:mentions: n3:11479625

Subject Item: _:vb29675223
rdf:type: n2:Context
rdf:value: However, these human-murine chimeric liver models lack a functional human immune system, thus it is not possible to study host immune response and hepatitis virus-induced immunopathology [14], [>>17<<]. To overcome the limitations associated with current chimeric human-murine liver mouse models, we have recently developed a humanized mouse model with both human immune system and liver cells (AFC8-hu HSC/Hep mice) [18], [19]. AFC8-hu
n2:mentions: n3:20179355

Subject Item: _:vb29675224
rdf:type: n2:Context
rdf:value: To overcome the limitations associated with current chimeric human-murine liver mouse models, we have recently developed a humanized mouse model with both human immune system and liver cells (AFC8-hu HSC/Hep mice) [>>18<<], [19]. AFC8-hu HSC/Hep mice can support HCV infection in the liver and generate human T-cell response to HCV. Additionally, HCV infection induces liver inflammation and fibrosis, correlated with activation of human hepatic stellate cells
n2:mentions: n3:21237170

Subject Item: _:vb29675225
rdf:type: n2:Context
rdf:value: To overcome the limitations associated with current chimeric human-murine liver mouse models, we have recently developed a humanized mouse model with both human immune system and liver cells (AFC8-hu HSC/Hep mice) [18], [>>19<<]. AFC8-hu HSC/Hep mice can support HCV infection in the liver and generate human T-cell response to HCV. Additionally, HCV infection induces liver inflammation and fibrosis, correlated with activation of human hepatic stellate cells and
n2:mentions: n3:21616105

Subject Item: _:vb29675226
rdf:type: n2:Context
rdf:value: Additionally, HCV infection induces liver inflammation and fibrosis, correlated with activation of human hepatic stellate cells and expression of human fibrogenic genes [>>18<<].
n2:mentions: n3:21237170

Subject Item: _:vb29675227
rdf:type: n2:Context
rdf:value: Several reports suggest that HBV promotes macrophage activation and M2 polarization [>>20<<], [21], [22].
n2:mentions: n3:23585678

Subject Item: _:vb29675228
rdf:type: n2:Context
rdf:value: Several reports suggest that HBV promotes macrophage activation and M2 polarization [20], [>>21<<], [22]. Macrophages play a critical role in modulating pathogen clearance, chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host
n2:mentions: n3:23024774

Subject Item: _:vb29675229
rdf:type: n2:Context
rdf:value: Several reports suggest that HBV promotes macrophage activation and M2 polarization [20], [21], [>>22<<]. Macrophages play a critical role in modulating pathogen clearance, chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity
n2:mentions: n3:9010683

Subject Item: _:vb29675230
rdf:type: n2:Context
rdf:value: pathogen clearance, chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity and promoting tissue fibrosis/remodeling [>>23<<], [24], [25], [26], [27].
n2:mentions: n3:22777483

Subject Item: _:vb29675231
rdf:type: n2:Context
rdf:value: clearance, chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity and promoting tissue fibrosis/remodeling [23], [>>24<<], [25], [26], [27].
n2:mentions: n3:23182716

Subject Item: _:vb29675232
rdf:type: n2:Context
rdf:value: clearance, chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity and promoting tissue fibrosis/remodeling [23], [24], [>>25<<], [26], [27].
n2:mentions: n3:23121638

Subject Item: _:vb29675233
rdf:type: n2:Context
rdf:value: chronic inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity and promoting tissue fibrosis/remodeling [23], [24], [25], [>>26<<], [27].
n2:mentions: n3:22699204

Subject Item: _:vb29675234
rdf:type: n2:Context
rdf:value: inflammation and associated liver pathology; with M1 polarized macrophages promoting pathogen clearance, and M2-like polarized macrophages impairing host immunity and promoting tissue fibrosis/remodeling [23], [24], [25], [26], [>>27<<].
n2:mentions: n3:22116397

Subject Item: _:vb29675235
rdf:type: n2:Context
rdf:value: a humanized mouse model by injecting human liver progenitor cells (Hep) and CD34+ human hematopoietic stem cells (HSC) directly into the liver of newborn A2/NSG (HLA-A2 transgenic NOD scid IL2 receptor gamma chain knockout mice [>>28<<], [29], [30]). The A2/NSG mouse lacks NK cells and T/B-lymphocytes. They support efficient development of a functional human immune system after injecting CD34+ human hematopoietic stem cells (HSC) into the liver of newborn mice [30], [31].
n2:mentions: n3:21429805

Subject Item: _:vb29675236
rdf:type: n2:Context
rdf:value: a humanized mouse model by injecting human liver progenitor cells (Hep) and CD34+ human hematopoietic stem cells (HSC) directly into the liver of newborn A2/NSG (HLA-A2 transgenic NOD scid IL2 receptor gamma chain knockout mice [28], [>>29<<], [30]). The A2/NSG mouse lacks NK cells and T/B-lymphocytes. They support efficient development of a functional human immune system after injecting CD34+ human hematopoietic stem cells (HSC) into the liver of newborn mice [30], [31].
n2:mentions: n3:20668220

Subject Item: _:vb29675237
rdf:type: n2:Context
rdf:value: mouse model by injecting human liver progenitor cells (Hep) and CD34+ human hematopoietic stem cells (HSC) directly into the liver of newborn A2/NSG (HLA-A2 transgenic NOD scid IL2 receptor gamma chain knockout mice [28], [29], [>>30<<]). The A2/NSG mouse lacks NK cells and T/B-lymphocytes. They support efficient development of a functional human immune system after injecting CD34+ human hematopoietic stem cells (HSC) into the liver of newborn mice [30], [31].
n2:mentions: n3:20615947

Subject Item: _:vb29675238
rdf:type: n2:Context
rdf:value: They support efficient development of a functional human immune system after injecting CD34+ human hematopoietic stem cells (HSC) into the liver of newborn mice [>>30<<], [31]. Furthermore, the A2/NSG mouse carries the human HLA-A2 transgene, which enhances development of human MHC-restrict T lymphocytes [30]. To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine
n2:mentions: n3:20615947

Subject Item: _:vb29675239
rdf:type: n2:Context
rdf:value: They support efficient development of a functional human immune system after injecting CD34+ human hematopoietic stem cells (HSC) into the liver of newborn mice [30], [>>31<<]. Furthermore, the A2/NSG mouse carries the human HLA-A2 transgene, which enhances development of human MHC-restrict T lymphocytes [30]. To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific
n2:mentions: n3:15064419

Subject Item: _:vb29675240
rdf:type: n2:Context
rdf:value: Furthermore, the A2/NSG mouse carries the human HLA-A2 transgene, which enhances development of human MHC-restrict T lymphocytes [>>30<<]. To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [32], [33], [34], [35], [36]. The A2/NSG-hu HSC/Hep mouse model enabled human liver and immune system
n2:mentions: n3:20615947

Subject Item: _:vb29675241
rdf:type: n2:Context
rdf:value: To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [>>32<<], [33], [34], [35], [36].
n2:mentions: n3:16497212

Subject Item: _:vb29675242
rdf:type: n2:Context
rdf:value: To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [32], [>>33<<], [34], [35], [36].
n2:mentions: n3:18714670

Subject Item: _:vb29675243
rdf:type: n2:Context
rdf:value: To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [32], [33], [>>34<<], [35], [36].
n2:mentions: n3:11124814

Subject Item: _:vb29675244
rdf:type: n2:Context
rdf:value: To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [32], [33], [34], [>>35<<], [36]. The A2/NSG-hu HSC/Hep mouse model enabled human liver and immune system development and supported long-term HBV infection, anti-HBV human immune response and HBV-induced liver diseases including hepatitis and fibrosis.
n2:mentions: n3:9040012

Subject Item: _:vb29675245
rdf:type: n2:Context
rdf:value: To promote human liver cell repopulation, A2/NSG-hu HSC/Hep mice were treated with a murine specific anti-Fas agonistic antibody (Jo2) [32], [33], [34], [35], [>>36<<]. The A2/NSG-hu HSC/Hep mouse model enabled human liver and immune system development and supported long-term HBV infection, anti-HBV human immune response and HBV-induced liver diseases including hepatitis and fibrosis. Interestingly, we
n2:mentions: n3:9771754

Subject Item: _:vb29675246
rdf:type: n5:Section
dc:title: materials and methods
n5:contains: _:vb29675260 _:vb29675261 _:vb29675262 _:vb29675263 _:vb29675256 _:vb29675257 _:vb29675258 _:vb29675259 _:vb29675252 _:vb29675253 _:vb29675254 _:vb29675255 _:vb29675248 _:vb29675249 _:vb29675250 _:vb29675251 _:vb29675247

Subject Item: _:vb29675247
rdf:type: n2:Context
rdf:value: Liver gene expression profile analyses in patients were obtained from a dataset in Gene Expression Omnibus (GEO)/NCBI database; the reports followed NIH research ethics guidelines [>>8<<], [9].
n2:mentions: n3:23185381

Subject Item: _:vb29675248
rdf:type: n2:Context
rdf:value: Liver gene expression profile analyses in patients were obtained from a dataset in Gene Expression Omnibus (GEO)/NCBI database; the reports followed NIH research ethics guidelines [8], [>>9<<].
n2:mentions: n3:20421498

Subject Item: _:vb29675249
rdf:type: n2:Context
rdf:value: Human liver progenitor cells containing hepatoblasts (Hep) and CD34+ hematopoietic stem cells (HSC) were isolated from 15–19 weeks old human fetal liver tissue (Advanced Bioscience Resources) essentially as described [>>56<<], [57], [58]. To separate progenitor liver cells from non-parenchymal cells (including HSC), the fetal liver cells were centrifuged at low speed three times (5 minutes, 18×g).
n2:mentions: n3:18544681

Subject Item: _:vb29675250
rdf:type: n2:Context
rdf:value: Human liver progenitor cells containing hepatoblasts (Hep) and CD34+ hematopoietic stem cells (HSC) were isolated from 15–19 weeks old human fetal liver tissue (Advanced Bioscience Resources) essentially as described [56], [>>57<<], [58]. To separate progenitor liver cells from non-parenchymal cells (including HSC), the fetal liver cells were centrifuged at low speed three times (5 minutes, 18×g).
n2:mentions: n3:16627685

Subject Item: _:vb29675251
rdf:type: n2:Context
rdf:value: Human liver progenitor cells containing hepatoblasts (Hep) and CD34+ hematopoietic stem cells (HSC) were isolated from 15–19 weeks old human fetal liver tissue (Advanced Bioscience Resources) essentially as described [56], [57], [>>58<<]. To separate progenitor liver cells from non-parenchymal cells (including HSC), the fetal liver cells were centrifuged at low speed three times (5 minutes, 18×g).
n2:mentions: n3:17132723

Subject Item: _:vb29675252
rdf:type: n2:Context
rdf:value: Animals were injected 3–5 times via ip with Jo2 antibody/PBS at 0.1–0.15 mg/kg body weight (BD Pharmingen) every 4–5 days at approximately 3–4 weeks post transplant of human cells [>>59<<]. At 12–16 weeks post-transplant with HSC+Hep cells, Transplanted mice were bled to determine human leukocyte (hCD45+) reconstitution by FACS and human albumin concentration in the blood by ELISA (Bethyl laboratories). All experiments
n2:mentions: n3:15965483

Subject Item: _:vb29675253
rdf:type: n2:Context
rdf:value: HBV serum genome was detected at termination using real-time PCR [>>60<<]. Serum cytokine levels were measure using a multiplex human cytokine array and following manufacturer's recommended procedures (Luminex, Millipore).
n2:mentions: n3:17373736

Subject Item: _:vb29675254
rdf:type: n2:Context
rdf:value: RNA was isolated from tissue following manufacturer's recommended procedures and qPCR was performed using species-specific published [>>18<<], [61] or NCBI primer blast generated primers and the SYBR Green method, following manufacturer's recommended procedures (Thermo Scientific).
n2:mentions: n3:21237170

Subject Item: _:vb29675255
rdf:type: n2:Context
rdf:value: RNA was isolated from tissue following manufacturer's recommended procedures and qPCR was performed using species-specific published [18], [>>61<<] or NCBI primer blast generated primers and the SYBR Green method, following manufacturer's recommended procedures (Thermo Scientific).
n2:mentions: n3:19041311

Subject Item: _:vb29675256
rdf:type: n2:Context
rdf:value: Immunoreactivity was determined by incubation with DAB substrate (Pierce) or Vulcan red (Dako), and counterstained with hematoxilin [>>56<<], [58]. Liver histological activity was determined using the knodell score, which examines liver necrosis, degeneration, inflammation and fibrosis [62], [63].
n2:mentions: n3:18544681

Subject Item: _:vb29675257
rdf:type: n2:Context
rdf:value: Immunoreactivity was determined by incubation with DAB substrate (Pierce) or Vulcan red (Dako), and counterstained with hematoxilin [56], [>>58<<]. Liver histological activity was determined using the knodell score, which examines liver necrosis, degeneration, inflammation and fibrosis [62], [63].
n2:mentions: n3:17132723

Subject Item: _:vb29675258
rdf:type: n2:Context
rdf:value: Liver histological activity was determined using the knodell score, which examines liver necrosis, degeneration, inflammation and fibrosis [>>62<<], [63].
n2:mentions: n3:7308988

Subject Item: _:vb29675259
rdf:type: n2:Context
rdf:value: Liver histological activity was determined using the knodell score, which examines liver necrosis, degeneration, inflammation and fibrosis [62], [>>63<<].
n2:mentions: n3:3338723

Subject Item: _:vb29675260
rdf:type: n2:Context
rdf:value: All patients were diagnosed according to our previously described criteria [>>64<<], [65] and had not received any antiviral therapies or immunosuppressive drugs within six months before sampling.
n2:mentions: n3:19788691

Subject Item: _:vb29675261
rdf:type: n2:Context
rdf:value: All patients were diagnosed according to our previously described criteria [64], [>>65<<] and had not received any antiviral therapies or immunosuppressive drugs within six months before sampling.
n2:mentions: n3:17052956

Subject Item: _:vb29675262
rdf:type: n2:Context
rdf:value: 17 different liver specimens approximately evenly taken from the 4 livers) and match healthy control liver donors (n = 10); acute HBV- induced liver failure patients were previously healthy and had no signs of chronic liver disease [>>8<<]. Microarray dataset (GEO accession: GSE49656; [8]) was analyzed using GEOR (NCBI Software).
n2:mentions: n3:23185381

Subject Item: _:vb29675263
rdf:type: n2:Context
rdf:value: Microarray dataset (GEO accession: GSE49656; [>>8<<]) was analyzed using GEOR (NCBI Software).
n2:mentions: n3:23185381

Subject Item: _:vb29675264
rdf:type: n5:Section
dc:title: results
n5:contains: _:vb29675268 _:vb29675269 _:vb29675270 _:vb29675271 _:vb29675265 _:vb29675266 _:vb29675267 _:vb29675276 _:vb29675277 _:vb29675278 _:vb29675279 _:vb29675272 _:vb29675273 _:vb29675274 _:vb29675275 _:vb29675284 _:vb29675285 _:vb29675280 _:vb29675281 _:vb29675282 _:vb29675283

Subject Item: _:vb29675265
rdf:type: n2:Context
rdf:value: We confirmed the specie-specificity of Jo2 antibody [>>32<<] by incubating human liver cell line (HepG2) with Jo2 antibody.
n2:mentions: n3:16497212

Subject Item: _:vb29675266
rdf:type: n2:Context
rdf:value: However, antigen-specific IgG response was detected in only two of eight mice and at very low levels as reported in other human B cell studies with humanized mice [>>37<<]. To characterize anti-HBV human T cell immune response, HLA-A2 donor derived-leukocytes from the spleen and lymph nodes of mock- or HBV-infected humanized animals were collected and stimulated in vitro with PHA or A2-restricted HBV
n2:mentions: n3:23089398

Subject Item: _:vb29675267
rdf:type: n2:Context
rdf:value: Chronic HBV infection in patients is associated with chronic hepatitis and liver fibrosis, characterized by leukocyte infiltration and collagen deposition in portal/periportal regions of the liver [>>38<<]. To examine leukocyte infiltration and fibrosis in HBV infected liver of humanized mice, liver sections were examined at time of sacrifice.
n2:mentions: n3:23344543

Subject Item: _:vb29675268
rdf:type: n2:Context
rdf:value: Several studies have suggested liver specific T cell immune impairment in chronic HBV infection [>>5<<]. To characterize anti-HBV human T cell immune response in lymphoid and liver tissues, HLA-A2 donor derived-leukocytes from the spleen and lymph nodes or livers of mock-, HBV plus neutralizing antibody- or HBV-infected humanized animals
n2:mentions: n3:17520515

Subject Item: _:vb29675269
rdf:type: n2:Context
rdf:value: clearance, chronic inflammation and associated tissue pathology; with M1-like macrophages promoting pathogen clearance, and M2-like macrophages impairing Th1 immune response and promoting tissue fibrosis/remodeling/wound healing [>>40<<]. Immunohistochemical analysis of HBV associated liver inflammation in humanized mice showed high levels of human macrophages with predominately “M2-like” phenotype (hCD68high, hCD14high, hCD16low/medium, hCD163high, hCD206high,
n2:mentions: n3:21997792

Subject Item: _:vb29675270
rdf:type: n2:Context
rdf:value: suppressor cells expressing high levels of IL10, co-inhibitory molecules (B7-H4), while depleting L-arginine and down-regulating IL12, TNFα and co-stimulatory molecules (CD86); all factors critical for Th1 anti-viral immune response [>>41<<]. Analysis of liver inflammation in HBV infected humanized mice showed human M2 macrophages co-localized with human T cells (Figure 7C, Table S2).
n2:mentions: n3:22378047

Subject Item: _:vb29675271
rdf:type: n2:Context
rdf:value: disease accounts for the vast majority of HBV associated morbidity/mortality, acute HBV infection occasionally results in accelerated liver disease and liver failure with subsequent mortality in the absence of liver transplantation [>>8<<]. Analysis of liver gene expression profile in acute HBV-induced liver failure patients also showed increased macrophage infiltration (CD68 upregulation), up-regulation of M2-like macrophage genes (IL10RA - Interleukin 10 receptor alpha
n2:mentions: n3:23185381

Subject Item: _:vb29675272
rdf:type: n2:Context
rdf:value: AMAC1 - alternative macrophage activation-associated CC chemokine-1, IL10, B7-H4) and down-regulation or no change of M1-like macrophage genes (TNFα, iNOS, IL12p40) in HBV infected patients compared to healthy controls (Figure S8, S9) [>>8<<], [9]. Furthermore, liver gene expression profile analysis showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and
n2:mentions: n3:23185381

Subject Item: _:vb29675273
rdf:type: n2:Context
rdf:value: - alternative macrophage activation-associated CC chemokine-1, IL10, B7-H4) and down-regulation or no change of M1-like macrophage genes (TNFα, iNOS, IL12p40) in HBV infected patients compared to healthy controls (Figure S8, S9) [8], [>>9<<]. Furthermore, liver gene expression profile analysis showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and
n2:mentions: n3:20421498

Subject Item: _:vb29675274
rdf:type: n2:Context
rdf:value: expression profile analysis showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [>>42<<], [43], [44], S100A9high [45], [46]) (Figure S9) [8], [9].
n2:mentions: n3:20195207

Subject Item: _:vb29675275
rdf:type: n2:Context
rdf:value: profile analysis showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [>>43<<], [44], S100A9high [45], [46]) (Figure S9) [8], [9].
n2:mentions: n3:18952078

Subject Item: _:vb29675276
rdf:type: n2:Context
rdf:value: profile analysis showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [43], [>>44<<], S100A9high [45], [46]) (Figure S9) [8], [9].
n2:mentions: n3:17853945

Subject Item: _:vb29675277
rdf:type: n2:Context
rdf:value: showed M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [43], [44], S100A9high [>>45<<], [46]) (Figure S9) [8], [9].
n2:mentions: n3:22253789

Subject Item: _:vb29675278
rdf:type: n2:Context
rdf:value: M2-like macrophage gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [43], [44], S100A9high [45], [>>46<<]) (Figure S9) [8], [9].
n2:mentions: n3:23977231

Subject Item: _:vb29675279
rdf:type: n2:Context
rdf:value: gene expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [43], [44], S100A9high [45], [46]) (Figure S9) [>>8<<], [9].
n2:mentions: n3:23185381

Subject Item: _:vb29675280
rdf:type: n2:Context
rdf:value: expression profile (CD68high, CD163high, AMAC1high, iNOSlow, TNFαlow) is associated with upregulation of tissue fibrosis (COL1A1high, TIMP1high) and damage markers (HMGB1high [42], [43], [44], S100A9high [45], [46]) (Figure S9) [8], [>>9<<].
n2:mentions: n3:20421498

Subject Item: _:vb29675281
rdf:type: n2:Context
rdf:value: Results from several cell culture studies have suggested that HBV can modulate monocyte activation resulting in induction of M2 associated cytokines and inhibition of M1 associated cytokines [>>20<<], [22], [47], [48], [49].
n2:mentions: n3:23585678

Subject Item: _:vb29675282
rdf:type: n2:Context
rdf:value: Results from several cell culture studies have suggested that HBV can modulate monocyte activation resulting in induction of M2 associated cytokines and inhibition of M1 associated cytokines [20], [>>22<<], [47], [48], [49].
n2:mentions: n3:9010683

Subject Item: _:vb29675283
rdf:type: n2:Context
rdf:value: Results from several cell culture studies have suggested that HBV can modulate monocyte activation resulting in induction of M2 associated cytokines and inhibition of M1 associated cytokines [20], [22], [>>47<<], [48], [49].
n2:mentions: n3:12270119

Subject Item: _:vb29675284
rdf:type: n2:Context
rdf:value: Results from several cell culture studies have suggested that HBV can modulate monocyte activation resulting in induction of M2 associated cytokines and inhibition of M1 associated cytokines [20], [22], [47], [>>48<<], [49]. Here we demonstrate that HBV viral stock promoted M2-like macrophage activation in both human M1 and M2 polarized macrophages as examined by the induction of spindle/fibroblast shaped morphology (as opposed to round/oval shaped
n2:mentions: n3:15963597

Subject Item: _:vb29675285
rdf:type: n2:Context
rdf:value: Results from several cell culture studies have suggested that HBV can modulate monocyte activation resulting in induction of M2 associated cytokines and inhibition of M1 associated cytokines [20], [22], [47], [48], [>>49<<]. Here we demonstrate that HBV viral stock promoted M2-like macrophage activation in both human M1 and M2 polarized macrophages as examined by the induction of spindle/fibroblast shaped morphology (as opposed to round/oval shaped
n2:mentions: n3:12029142

Subject Item: _:vb29675286
rdf:type: n5:Section
dc:title: discussion
n5:contains: _:vb29675308 _:vb29675309 _:vb29675304 _:vb29675305 _:vb29675306 _:vb29675307 _:vb29675300 _:vb29675301 _:vb29675302 _:vb29675303 _:vb29675296 _:vb29675297 _:vb29675298 _:vb29675299 _:vb29675292 _:vb29675293 _:vb29675294 _:vb29675295 _:vb29675288 _:vb29675289 _:vb29675290 _:vb29675291 _:vb29675287

Subject Item: _:vb29675287
rdf:type: n2:Context
rdf:value: Immunodeficient mice expressing the uPA transgene in the liver of SCID mice or with mutant Fah genes allow transplanted human adult hepatocytes to have a growth advantage and efficiently repopulate the liver [>>50<<]. However, these mice have disadvantages including neonatal death, poor health and, most importantly, the lack of a human immune system [19].
n2:mentions: n3:18706933

Subject Item: _:vb29675288
rdf:type: n2:Context
rdf:value: However, these mice have disadvantages including neonatal death, poor health and, most importantly, the lack of a human immune system [>>19<<]. To overcome these deficiencies, the A2/NSG/Fas-humanized mouse model enables inducible depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with
n2:mentions: n3:21616105

Subject Item: _:vb29675289
rdf:type: n2:Context
rdf:value: mouse model enables inducible depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with human liver progenitor and hematopoietic stem cells [>>32<<], [33], [34], [36], [51]. Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [52].
n2:mentions: n3:16497212

Subject Item: _:vb29675290
rdf:type: n2:Context
rdf:value: model enables inducible depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with human liver progenitor and hematopoietic stem cells [32], [>>33<<], [34], [36], [51]. Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [52].
n2:mentions: n3:18714670

Subject Item: _:vb29675291
rdf:type: n2:Context
rdf:value: enables inducible depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with human liver progenitor and hematopoietic stem cells [32], [33], [>>34<<], [36], [51]. Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [52].
n2:mentions: n3:11124814

Subject Item: _:vb29675292
rdf:type: n2:Context
rdf:value: inducible depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with human liver progenitor and hematopoietic stem cells [32], [33], [34], [>>36<<], [51]. Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [52].
n2:mentions: n3:9771754

Subject Item: _:vb29675293
rdf:type: n2:Context
rdf:value: depletion of murine hepatocytes through the Fas apoptotic signaling pathway, resulting in elevated human liver repopulation in mice transplanted with human liver progenitor and hematopoietic stem cells [32], [33], [34], [36], [>>51<<]. Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [52].
n2:mentions: n3:12810955

Subject Item: _:vb29675294
rdf:type: n2:Context
rdf:value: Additionally, the A2/NSG background permits highly efficient engraftment and development of human xenografts including human hematopoietic stem cells compared to current immunodeficient mouse models [>>52<<]. Lower levels of human hepatocytes were detected in A2/NSG/Fas-humanized mice in comparison to the uPA or FAH mice transplanted with adult human hepatocytes. However, it should be noted that fetal liver cell repopulation is also low in
n2:mentions: n3:17259968

Subject Item: _:vb29675295
rdf:type: n2:Context
rdf:value: However, it should be noted that fetal liver cell repopulation is also low in those mouse models [>>53<<]. Genetic modification of human liver cells for enhanced survival, repopulation and differentiation coupled with mouse Fas agonist (Jo2) [34] and/or the AFC8 murine liver damage system [18] could further enhance human liver repopulation.
n2:mentions: n3:19717639

Subject Item: _:vb29675296
rdf:type: n2:Context
rdf:value: Genetic modification of human liver cells for enhanced survival, repopulation and differentiation coupled with mouse Fas agonist (Jo2) [>>34<<] and/or the AFC8 murine liver damage system [18] could further enhance human liver repopulation.
n2:mentions: n3:11124814

Subject Item: _:vb29675297
rdf:type: n2:Context
rdf:value: Genetic modification of human liver cells for enhanced survival, repopulation and differentiation coupled with mouse Fas agonist (Jo2) [34] and/or the AFC8 murine liver damage system [>>18<<] could further enhance human liver repopulation.
n2:mentions: n3:21237170

Subject Item: _:vb29675298
rdf:type: n2:Context
rdf:value: However, only suboptimal B cell response has been reported thus far in humanized mouse models [>>52<<]. In concordance with those studies, we detected predominantly human IgM antibodies with anti-HBV activity in HBV infected animals. Although human lymphoid T cells exhibited robust anti-HBV immune responses, HBV infection resulted in
n2:mentions: n3:17259968

Subject Item: _:vb29675299
rdf:type: n2:Context
rdf:value: In chronically infected patients, immune and inflammatory responses against HBV are implicated as the major mediators of liver diseases [>>54<<], [55]. Chronic HBV infection in the liver of A2/NSG/Fas-hu mice was associated with significant human leukocyte infiltration, leading to human hepatic stellate cell activation and human liver fibrosis.
n2:mentions: n3:22163270

Subject Item: _:vb29675300
rdf:type: n2:Context
rdf:value: In chronically infected patients, immune and inflammatory responses against HBV are implicated as the major mediators of liver diseases [54], [>>55<<]. Chronic HBV infection in the liver of A2/NSG/Fas-hu mice was associated with significant human leukocyte infiltration, leading to human hepatic stellate cell activation and human liver fibrosis.
n2:mentions: n3:22155900

Subject Item: _:vb29675301
rdf:type: n2:Context
rdf:value: and associated tissue fibrosis and damage; with M1 polarized macrophages promoting anti-virus Th1 immune response and pathogen clearance, while M2 polarized macrophages impair Th1 immune response and promoting tissue remodeling [>>23<<], [24], [25], [26], [27].
n2:mentions: n3:22777483

Subject Item: _:vb29675302
rdf:type: n2:Context
rdf:value: and associated tissue fibrosis and damage; with M1 polarized macrophages promoting anti-virus Th1 immune response and pathogen clearance, while M2 polarized macrophages impair Th1 immune response and promoting tissue remodeling [23], [>>24<<], [25], [26], [27].
n2:mentions: n3:23182716

Subject Item: _:vb29675303
rdf:type: n2:Context
rdf:value: tissue fibrosis and damage; with M1 polarized macrophages promoting anti-virus Th1 immune response and pathogen clearance, while M2 polarized macrophages impair Th1 immune response and promoting tissue remodeling [23], [24], [>>25<<], [26], [27].
n2:mentions: n3:23121638

Subject Item: _:vb29675304
rdf:type: n2:Context
rdf:value: tissue fibrosis and damage; with M1 polarized macrophages promoting anti-virus Th1 immune response and pathogen clearance, while M2 polarized macrophages impair Th1 immune response and promoting tissue remodeling [23], [24], [25], [>>26<<], [27]. M2 macrophages are critical innate immune cells involved in tissue remodeling/wound repair, secreting anti-inflammatory cytokines and redistributing micronutrients to sites of wound repair; however, during chronic infection,
n2:mentions: n3:22699204

Subject Item: _:vb29675305
rdf:type: n2:Context
rdf:value: fibrosis and damage; with M1 polarized macrophages promoting anti-virus Th1 immune response and pathogen clearance, while M2 polarized macrophages impair Th1 immune response and promoting tissue remodeling [23], [24], [25], [26], [>>27<<]. M2 macrophages are critical innate immune cells involved in tissue remodeling/wound repair, secreting anti-inflammatory cytokines and redistributing micronutrients to sites of wound repair; however, during chronic infection, M2-like
n2:mentions: n3:22116397

Subject Item: _:vb29675306
rdf:type: n2:Context
rdf:value: micronutrients to sites of wound repair; however, during chronic infection, M2-like macrophages promote tissue fibrosis, neoplasia and impair Th1 response thus promoting pathogen persistence and associated tissue pathology [>>40<<]. We report that liver inflammation and immune impairment in chronic HBV infected humanized mice livers was associated with M2-like macrophages, which also localized to fibrotic regions.
n2:mentions: n3:21997792

Subject Item: _:vb29675307
rdf:type: n2:Context
rdf:value: Several studies have reported that HBV virus/HBV-encoded proteins can directly promote M2-like activation [>>20<<], [21], [22].
n2:mentions: n3:23585678

Subject Item: _:vb29675308
rdf:type: n2:Context
rdf:value: Several studies have reported that HBV virus/HBV-encoded proteins can directly promote M2-like activation [20], [>>21<<], [22]. We confirmed and extended those results by demonstrating that HBV promotes M2 macrophage polarization in human M1 and M2 macrophages.
n2:mentions: n3:23024774

Subject Item: _:vb29675309
rdf:type: n2:Context
rdf:value: Several studies have reported that HBV virus/HBV-encoded proteins can directly promote M2-like activation [20], [21], [>>22<<]. We confirmed and extended those results by demonstrating that HBV promotes M2 macrophage polarization in human M1 and M2 macrophages.
n2:mentions: n3:9010683

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