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  • 1
    Online Resource
    Online Resource
    Clinical-Scale Isolation of Interleukin-2-Stimulated Liver Natural Killer Cells for Treatment of Liver Transplantation with Hepatocellular Carcinoma
    SAGE Publications ; 2012
    In:  Cell Transplantation Vol. 21, No. 7 ( 2012-07), p. 1397-1406
    Details
    In: Cell Transplantation, SAGE Publications, Vol. 21, No. 7 ( 2012-07), p. 1397-1406
    Abstract: Tumor recurrence is the main limitation of liver transplantation (LT) in patients with hepatocellular carcinoma (HCC) and can be promoted by immunosuppressants. However, there is no prevention or treatment for HCC recurrence after LT. Here we describe a clinical-scale method for an adoptive immunotherapy approach that uses natural killer (NK) cells derived from deceased donor liver graft perfusate to prevent tumor recurrence after LT. Liver mononuclear cells (LMNCs) that were extracted from deceased donor liver graft perfusate contained a high percentage of NK cells (45.0 ± 4.0%) compared with peripheral blood mononuclear cells (PBMCs) (21.8 ± 5.2%) from the same donor. The CD69 activation marker and the natural cytotoxicity receptors, NKp44 and NKp46, were expressed at high levels in freshly isolated liver NK cells. Furthermore, interleukin-2 (IL-2)-stimulated NK cells showed greater upregulation of activation markers and the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is critical for NK cell-mediated antitumor cell death and increased production of interferon. Moreover, IL-2 stimulation induced LMNCs to exhibit a strong cytotoxicity against NK-susceptible K562 target cells compared with PBMCs ( p 〈 0.01). Finally, we also showed that the final product contained a very low T-cell contamination (0.02 ± 10 6 cells/kg −1 ), which reduces the risk of graft-versus-host disease (GVHD). Collectively, our results suggest that the adoptive transfer of IL-2-stimulated NK cells from deceased donor liver graft perfusate could be a promising treatment for LT patients with HCC.
    Type of Medium: Online Resource
    ISSN: 0963-6897 , 1555-3892
    URL: Article
    DOI: 10.3727/096368911X627589
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
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  • 2
    Online Resource
    Online Resource
    In Response
    SAGE Publications ; 1995
    In:  Vascular Surgery Vol. 29, No. 4 ( 1995-07), p. 342-342
    Details
    In: Vascular Surgery, SAGE Publications, Vol. 29, No. 4 ( 1995-07), p. 342-342
    Type of Medium: Online Resource
    ISSN: 0042-2835
    URL: Article
    DOI: 10.1177/153857449502900417
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1995
    detail.hit.zdb_id: 2095223-5
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  • 3
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    Online Resource
    Human CD47 Expression Permits Survival of Porcine Cells in Immunodeficient Mice that Express SIRPα Capable of Binding to Human CD47
    SAGE Publications ; 2011
    In:  Cell Transplantation Vol. 20, No. 11-12 ( 2011-12), p. 1915-1920
    Details
    In: Cell Transplantation, SAGE Publications, Vol. 20, No. 11-12 ( 2011-12), p. 1915-1920
    Abstract: Signal regulatory protein α (SIRPα) is a critical immune inhibitory receptor on macrophages, and its interaction with CD47 prevents autologous phagocytosis. We have previously shown that pig CD47 does not interact with human SIRPα, and that human CD47 expression inhibits phagocytosis of porcine cells by human macrophages in vitro. In this study, we have investigated the potential of human CD47 expression to promote porcine cell survival in vivo. Human CD47-expressing and control porcine B-lymphoma cells were transplanted into T- and B-cell-deficient nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice that express SIRPα capable of interacting with human CD47. Only the human CD47-expressing porcine lymphoma cells survived and were able to form tumors in NOD/SCID mice; however, both the control and human CD47-expressing porcine cells survived in macrophage-depleted NOD/SCID mice. These results indicate that transgenic expression of human CD47 may provide an effective approach to inhibiting macrophage-mediated xenograft rejection in clinical xenotransplantation.
    Type of Medium: Online Resource
    ISSN: 0963-6897 , 1555-3892
    URL: Article
    DOI: 10.3727/096368911X566253
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
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  • 4
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    Online Resource
    Adoptive Transfer of Allogeneic Liver Sinusoidal Endothelial Cells Specifically Inhibits T-Cell Responses to Cognate Stimuli
    SAGE Publications ; 2013
    In:  Cell Transplantation Vol. 22, No. 9 ( 2013-09), p. 1695-1708
    Details
    In: Cell Transplantation, SAGE Publications, Vol. 22, No. 9 ( 2013-09), p. 1695-1708
    Abstract: Although it is well known that liver allografts are often accepted by recipients, leading to donor-specific tolerance of further organ transplants, the underlying mechanisms remain unclear. We had previously used an in vitro model and showed that mouse liver sinusoidal endothelial cells (LSECs) selectively suppress allospecific T-cells across major histocompatibility complex (MHC) barriers. In the present study, we established an in vivo model for evaluating the immunomodulatory effects of allogeneic LSECs on corresponding T-cells. Allogeneic BALB/cA LSECs were injected intraportally into recombination activating gene 2 γ-chain double-knockout (RAG2/gc-KO, H-2 b ) mice lacking T, B, and natural killer (NK) cells. In order to facilitate LSEC engraftment, the RAG2/gc-KO mice were injected intraperitoneally with monocrotaline 2 days before the adoptive transfer of LSECs; this impaired the host LSECs, conferring a proliferative advantage to the transplanted LSECs. After orthotopic allogeneic LSEC engraftment, the RAG2/gc-KO mice were immune reconstituted intravenously with C57BL/6 splenocytes. After immune reconstitution, mixed lymphocyte reaction (MLR) assay using splenocytes from the recipients revealed that specific inhibition of host CD4 + and CD8 + T-cell proliferation was greater in response to allostimulation with irradiated BALB/cA splenocytes rather than to stimulation with irradiated third party SJL/jorllco splenocytes. This inhibitory effect was attenuated by administering anti-programmed death ligand 1 (PD-L1) monoclonal antibody during immune reconstitution in the above-mentioned mice, but not in RAG2/gc-KO mice engrafted with Fas ligand (FasL)-deficient BALB/cA LSECs. Furthermore, engraftment of allogeneic BALB/cA LSECs significantly prolonged the survival of subsequently grafted cognate allogeneic BALB/cA hearts in RAG2/gc-KO mice immune reconstituted with bone marrow transplantation from C57BL/6 mice. In conclusion, murine LSECs have been proven capable of suppressing T-cells with cognate specificity for LSECs in an in vivo model. The programmed death 1/PD-L1 pathway is likely involved in these suppressive effects.
    Type of Medium: Online Resource
    ISSN: 0963-6897 , 1555-3892
    URL: Article
    DOI: 10.3727/096368912X657738
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2013
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  • 5
    Online Resource
    Online Resource
    Leiomyosarcoma of the Inferior Vena Cava : A Case Report of Steroid-Receptors-Positive Leiomyosarcoma
    SAGE Publications ; 1994
    In:  Vascular Surgery Vol. 28, No. 4 ( 1994-05), p. 289-294
    Details
    In: Vascular Surgery, SAGE Publications, Vol. 28, No. 4 ( 1994-05), p. 289-294
    Abstract: A case of a thirty-nine-year-old woman with leiomyosarcoma of the inferior vena cava (IVC) is described. The tumor arose from the middle segment of the IVC, and liver metastasis of the tumor was found. The tissue of the tumor obtained at laparotomy was positive for estrogen receptor and progesterone receptor. The patient has been treated with combined multimodal therapy including resection of the main tumor, intrahepato-arterial chemotherapy, and hormonal manipulation. To the authors' knowledge, this is the first case of leiomyosarcoma of the IVC in which the presence of steroid receptors was determined.
    Type of Medium: Online Resource
    ISSN: 0042-2835
    URL: Article
    DOI: 10.1177/153857449402800407
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1994
    detail.hit.zdb_id: 2095223-5
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  • 6
    Online Resource
    Online Resource
    Risk Factors for Hepatocellular Carcinoma After Splenectomy in Liver Cirrhotic Patients
    SAGE Publications ; 2023
    In:  The American Surgeon™ Vol. 89, No. 4 ( 2023-04), p. 769-777
    Details
    In: The American Surgeon™, SAGE Publications, Vol. 89, No. 4 ( 2023-04), p. 769-777
    Abstract: Splenectomy is sometimes indicated for portal hypertension caused by cirrhosis, which is a risk for hepatic carcinogenesis. This study aimed to identify risk factors for hepatocellular carcinoma (HCC) development after splenectomy. Methods This retrospective study included 65 patients who underwent splenectomy for portal hypertension between 2009 and 2017. Cox regression analyses were performed to identify factors related to HCC development after splenectomy. The predictive index for HCC development was constructed from the results of multivariate analysis, and 3 risk-dependent groups were defined. Discrimination among the groups was estimated using Kaplan-Meier curves and the log-rank test. Results Post-splenectomy, 36.9% of patients developed HCC. In the univariate analysis, the etiology of cirrhosis (hepatitis C virus antibody, P = .005, and hepatitis B surface antigen, P = .008, referring to non-B and non-C patients, respectively), presence of HCC history ( P 〈 .001), and preoperative hemoglobin level ( P = .007) were related to HCC development, and the presence of HCC history ( P = .002) and preoperative hemoglobin level ( P = .022) were independent risk factors. The predictive index classified three groups at risk; the hazards in each group were significantly different (low vs middle risk, P = .035, and middle vs high risk, P = .011). Discussion The etiology of cirrhosis, presence of HCC history, and hemoglobin level were associated with HCC development after splenectomy. The predictive model may aid in HCC surveillance after splenectomy for patients with portal hypertension.
    Type of Medium: Online Resource
    ISSN: 0003-1348 , 1555-9823
    URL: Article
    DOI: 10.1177/00031348211041562
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
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