Adhesion of Epstein–Barr virus-positive natural killer cell lines to cultured endothelial cells stimulated with inflammatory cytokines

Kanno, Hiroyuki; Watabe, Daisuke; Shimizu, Norio; Sawai, Takashi

doi:10.1111/j.1365-2249.2007.03584.x

Cited by 29 publications

(22 citation statements)

References 36 publications

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“…Previous studies have reported that ICAM-1 (CD54) is highly expressed on SNK6 [8,34]. In this study, we showed that the EBV-positive NK-cell lines SNK6 and KAI3, which are also positive for LMP-1, expressed LFA-1 at the cell surface ( Figure 1A).…”

Section: Discussionsupporting

confidence: 58%

Soluble ICAM-1 secretion and its functional role as an autocrine growth factor in nasal NK/T cell lymphoma cells

Takahara

Nagato

Komabayashi

et al. 2013

Experimental Hematology

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Section: Discussionsupporting

confidence: 58%

Soluble ICAM-1 secretion and its functional role as an autocrine growth factor in nasal NK/T cell lymphoma cells

Takahara

Nagato

Komabayashi

et al. 2013

Experimental Hematology

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“…SNK6 cells reportedly produce TNF-α [28], which activates NF-κB in T and NK cells. The serum TNF-α concentration was found to be significantly higher in patients with CAEBV than in healthy donors [29].…”

Section: Discussionmentioning

confidence: 99%

EBV induces persistent NF-κB activation and contributes to survival of EBV-positive neoplastic T- or NK-cells

et al. 2017

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Epstein–Barr virus (EBV) has been detected in several T- and NK-cell neoplasms such as extranodal NK/T-cell lymphoma nasal type, aggressive NK-cell leukemia, EBV-positive peripheral T-cell lymphoma, systemic EBV-positive T-cell lymphoma of childhood, and chronic active EBV infection (CAEBV). However, how this virus contributes to lymphomagenesis in T or NK cells remains largely unknown. Here, we examined NF-κB activation in EBV-positive T or NK cell lines, SNT8, SNT15, SNT16, SNK6, and primary EBV-positive and clonally proliferating T/NK cells obtained from the peripheral blood of patients with CAEBV. Western blotting, electrophoretic mobility shift assays, and immunofluorescent staining revealed persistent NF-κB activation in EBV-infected cell lines and primary cells from patients. Furthermore, we investigated the role of EBV in infected T cells. We performed an in vitro infection assay using MOLT4 cells infected with EBV. The infection directly induced NF-κB activation, promoted survival, and inhibited etoposide-induced apoptosis in MOLT4 cells. The luciferase assay suggested that LMP1 mediated NF-κB activation in MOLT4 cells. IMD-0354, a specific inhibitor of NF-κB that suppresses NF-κB activation in cell lines, inhibited cell survival and induced apoptosis. These results indicate that EBV induces NF-κB-mediated survival signals in T and NK cells, and therefore, may contribute to the lymphomagenesis of these cells.

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“…43 Moreover, SNT16 and SNK6 nonHodgkin lymphoma cells induced high levels of IL-2 production from CD70-specific T cells, an effect consistent with the known high expression of adhesion molecules on EBV-positive, NK/T-cell non-Hodgkin lymphoma cells. 44 CD27 costimulation prevents activation-induced cell death in T cells, in part by up-regulation of Bcl-xl, an antiapoptotic protein. 34 In agreement with this finding, we observed that T cells expressing ⌬CD70-CARs with a deleted CD27 costimulatory domain had decreased viability and lower levels of Bcl-xl expression than T cells expressing CD70-CARs with full-length CD27.…”

Section: T-cell Therapy Formentioning

confidence: 99%

T cells redirected against CD70 for the immunotherapy of CD70-positive malignancies

Shaffer

Savoldo

et al. 2011

Blood

150

100

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IntroductionImmunotherapy with antigen-specific T cells has shown promise in the treatment of hematologic malignancies in preclinical models and in phase 1/2 clinical studies. [1][2][3] One attractive strategy to generate tumor-specific T cells is by genetic modification with chimeric antigen receptors (CARs), which consist of an extracellular antigen-recognition domain, a transmembrane domain, and an intracellular signaling domain derived from the TCR CD3-chain often linked to costimulatory molecule endodomains. 4,5 CARs targeting CD19 and CD20 antigens for the treatment of hematologic malignancies have been explored extensively, but this approach is limited to B cell-derived malignancies and may produce prolonged impairment of humoral immunity because of the potentially long life span of T cells. 6,7 It is therefore desirable to prepare CARs directed against alternative antigens that could broaden the spectrum of potentially treatable tumors and/or potentially reduce damage to normal cells.CD70 is the membrane-bound ligand of the CD27 receptor, which belongs to the tumor necrosis factor receptor superfamily. 8,9 CD70 is expressed by diffuse large B-cell and follicular lymphoma and also by the malignant cells of Hodgkin lymphoma, Waldenström macroglobulinemia, and multiple myeloma, and by human T-lymphotropic virus type 1-and EBV-associated malignancies. [10][11][12][13][14] In addition, CD70 is expressed by nonhematologic malignancies such as renal cell carcinoma and glioblastoma. 15,16 Physiologically, CD70 expression is transient and restricted to a subset of highly activated T, B, and dendritic cells. Whereas CD70/CD27 costimulation plays a role in T-cell activation, CD70/ CD27 signaling is not essential for the development and maintenance of a functional immune system, because CD27-knockout mice have no overt immunodeficiency and recover from influenza virus infection within the same time frame as wild-type mice. 17,18 Targeting CD70-positive malignancies with CD70-specific monoclonal antibodies has shown promise in preclinical animal models, 14,19,20 and we have now evaluated whether T cells can be redirected to CD70 by forced expression of the appropriate CAR. Because CARs consist of an extracellular antigen-recognition domain derived from murine monoclonal antibodies, they may induce human anti-mouse antibody on infusion unless fully humanized. 21,22 One potential strategy to overcome this limitation is to engineer the antigen-recognition domain using endogenous protein ligands or receptors rather than monoclonal antibodies. 23,24 To target CD70 with T cells, we took advantage of the physiologic CD70/CD27 interaction and generated a CD70-specific CAR, which consists of full-length CD27 as the antigen-recognition domain fused to the intracellular domain of the CD3-chain. Engagement of chimeric CD27-by tumor targets expressing the CD70 ligand resulted in T-cell activation and CD27 costimulation, which was dependent on the presence of the TRAF2-binding site within the cytoplasmic tail of CD27. CD70-specifi...

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Adhesion of Epstein–Barr virus-positive natural killer cell lines to cultured endothelial cells stimulated with inflammatory cytokines

Abstract: Summary Chronic active Epstein-Barr virus (EBV) infection (CAEBV) is characterized

Cited by 29 publications

References 36 publications

Soluble ICAM-1 secretion and its functional role as an autocrine growth factor in nasal NK/T cell lymphoma cells

Soluble ICAM-1 secretion and its functional role as an autocrine growth factor in nasal NK/T cell lymphoma cells

EBV induces persistent NF-κB activation and contributes to survival of EBV-positive neoplastic T- or NK-cells

T cells redirected against CD70 for the immunotherapy of CD70-positive malignancies

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