Effective anti‐metastatic melanoma vaccination with tumor cells transfected with MHC genes and/or infected with newcastle disease virus (NDV)

Plaksin, Daniel; Porgador, Angel; Vadai, Ezra; Feldman, Michaël; Schirrmacher, Volker; Eisenbach, Lea

doi:10.1002/ijc.2910590615

Cited by 35 publications

(18 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…39 Similar results were obtained by von Hoegen et al, 16,17 who characterized the effects of NDV infection in a murine model using the highly metastatic murine lymphoma line ESb injected in immunocompetent syngenic DBA/2 mice. They demonstrated that spleen cells from mice immunized with NDV-infected ESb cells contain an enhanced immune capacity in both CD4 ϩ and CD8 ϩ T-cell compartments.…”

Section: Discussionsupporting

confidence: 81%

“…This is in accordance with the finding that NDV infection efficiently prevents the growth and micrometastasis of established B16 melanoma in immunocompetent mice only if these are MHC-matched. 39 Furthermore, lymphocytes play an essential role in NDV-mediated tumor lysis in vivo, because depletion of CD4 ϩ , CD8…”

Section: Discussionmentioning

confidence: 99%

“…There was no participation of either CD4 ϩ or CD8 ϩ virus-specific T cells in the augmented response, 18 ruling out the possibility that viral peptides presented by MHC on the surface of the tumor cells were responsible for the NDV effect. Nevertheless, Plaksin et al 39 indicated that specific immune recognition of a tumor Ag by the TCR of CD4…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Newcastle disease virus infection induces B7-1/B7-2-independent T-cell costimulatory activity in human melanoma cells

et al. 2000

Self Cite

View full text Add to dashboard Cite

Viral oncolysates of Newcastle disease virus (NDV) have been widely used for the treatment of malignant melanoma. Apparently, this nononcogenic and apathogenic paramyxovirus can alter the immunogenicity of tumor cells. To determine the influence of NDV infection on a tumor-specific T-cell response on a functional level, we used autologous primary melanoma cells infected with the NDV-strain Ulster. Therefore, melanoma cells and tumor-infiltrating lymphocytes were prepared from a freshly resected tumor, and tumor-infiltrating lymphocytes were subjected to limited dilution cloning. Proliferation assays of the T-helper cell clone sTS3 (CD4 ϩ )showed that the T-cell clone was rendered nonreactive against its autologous major histocompatibility complex II ϩ , B7-1/B7-2 Ϫ melanoma SMS, even remaining unresponsive to subsequent stimulation by interleukin-2. NDV infection of the SMS melanoma cell line not only completely restored the proliferative response of sTS3 to SMS, comparable with stimulation by cross-linking of anti-CD3/anti-CD28 monoclonal antibodies, but also inhibited the induction of anergy. Electrophoretic mobility shift assays of sTS3 cell lysates revealed the induction of the CD28-responsive complex by coincubation with NDV-infected melanoma cells. Because the induction of this complex of nuclear proteins shows specificity for the activation of the CD28 pathway but functional B7-1/B7-2 expression was not detectable on SMS melanoma cells at any timepoint, we propose the induction of a costimulatory factor different from B7 by NDV viral proteins. Cancer Gene Therapy (2000) 7, 316 -323

show abstract

Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Newcastle disease virus infection induces B7-1/B7-2-independent T-cell costimulatory activity in human melanoma cells

et al. 2000

Self Cite

View full text Add to dashboard Cite

show abstract

“…Indeed, herpes simplex virus 17 and vesicular stomatitis virus 8 appear to exert antitumoral immune responses in addition to their oncolytical effect. In a similar manner, herpes simplex virus, 17 vesicular stomatitis virus 8 and Newcastle disease virus 29 -infected tumor cells have been reported to activate antitumoral immunity. Previous studies with replication-competent adenovirus-infected carrier-cell systems have reported the use of wild-type HAd5 adenovirus-infected MDA-MG-231 cells 30 and also of granulocyte-macrophage colonystimulating factor-expressing HAd5 loaded into A549 and 293 cells.…”

Section: Discussionmentioning

confidence: 87%

Osteosarcoma cells as carriers to allow antitumor activity of canine oncolytic adenovirus in the presence of neutralizing antibodies

et al. 2010

View full text Add to dashboard Cite

Osteosarcoma (OSA) is the most common bone tumor affecting the dog. The veterinary options for therapeutic management of OSA are limited and prognosis for such patients is poor. Oncolytic adenoviruses are attractive tools for experimental therapeutics as they can replicate and spread within tumors to directly induce tumor destruction. However, a major impediment to systemic oncolytic adenoviruses injection is the presence of pre-existing neutralizing antibodies (Nabs). In this study, we investigated the effect of a replication-selective canine adenovirus (OCCAV) to treat OSA in the presence of Nabs and the use of canine OSA cells as carrier vehicles for evading Nabs. Our systemic biodistribution data indicated that canine tumor cells could successfully reach the tumor site and deliver OCCAV to tumor cells in an immunized mice model. Furthermore, the use of carrier cells also reduced adenovirus uptake by the liver. Importantly, OCCAV alone was not effective to control tumor growth in a pre-immunized xenograft mouse model. On the contrary, systemic antitumoral activity of carrier-cell OCCAV was evident even in the presence of circulating antibodies, which is a relevant result from a clinical point of view. These findings are of direct translational relevance for the future design of canine clinical trials.

show abstract

“…12 Postoperative vaccination with NDV-modified autologous tumor cell vaccine (ATV-NDV) was effective in vivo in various animal tumor models to prevent metastatic spread and to increase survival. 13,14 The mechanism of the immunopotentiating effect of this virus was analyzed in detail. [15][16][17] Since 1988, a comparable ATV-NDV was developed for clinical application.…”

mentioning

confidence: 99%

An effective strategy of human tumor vaccine modification by coupling bispecific costimulatory molecules

Haas

Herold‐Mende

Gerhards³

et al. 1999

Cancer Gene Ther

Self Cite

View full text Add to dashboard Cite

A new, generally applicable procedure is described for the introduction of defined costimulatory molecules into human cancer cells to increase their T-cell stimulatory capacity. The procedure involves infection with Newcastle disease virus to mediate the cell surface binding of costimulatory molecules (e.g., specially designed bispecific antibodies (bsAb)). The modification is independent of tumor cell proliferation and laborious recombinant gene technology and can be applied directly to freshly isolated and ␥-irradiated patient-derived tumor cells as an autologous cancer vaccine. Following the infection of tumor cells with a nonvirulent strain of Newcastle disease virus, the cells are washed and then further modified by coincubation with bsAbs, which attach with one arm to the viral hemagglutinin-neuraminidase (HN) molecule on the infected tumor cells. The second specificity of one bsAb (bs HN ϫ CD28) is directed against CD28 to augment antitumor T-cell responses by selectively channeling positive costimulatory signals via the CD28 pathway. A second bsAb (bs HN ϫ CD3) was produced to deliver T-cell receptor-mediated signals either alone (bsCD3 vaccine) or in combination with anti-CD28 (bsCD3 vaccine plus bsCD28 vaccine). In human T-cell stimulation studies in vitro, the bsCD28 vaccine caused an up-regulation of early (CD69) and late (CD25) T-cell activation markers on CD4 and CD8 T lymphocytes from either normal healthy donors or cancer patients (autologous system) and induced tumor cytostasis in nonmodified bystander tumor cells. In addition, in combination with the bsCD3 vaccine, augmented antitumor cytotoxicity and T-cell proliferative responses were observed. This tumor vaccine modification procedure is highly specific, quick, economic, and has a broad range of clinical applications. T here is now much evidence that an antigen (Ag)-specific, T-cell-mediated immune response requires, apart from the Ag, additional costimulatory signals. 1,2 These signals are normally provided by professional Ag-presenting cells (APCs) such as dendritic cells, macrophages, and activated B lymphocytes but not, for instance, by carcinoma cells, which represent the majority of human tumors and are derived from the non-APCtype cells that form the epithelial layers. In the absence of costimulation, encounters with a tumor-associated Ag (TAA) can lead to T-cell inactivation or death rather than to proliferation and differentiation into effector cells. Modern gene therapy strategies, therefore, aim at transforming carcinoma cells into professional APCs by transfecting genes that code for T-cell costimulatory molecules, such as CD80 (B7-1), 2,3 CD86 (B7-2), and/or cytokines. 4,5 In support of this concept, some nonimmunogenic transplantable tumor cells were shown to become immunogenic after CD80, CD86, and/or cytokine gene transfection, and mice that rejected such transfectants developed systemic protective immunity against the nontransfected tumor. [2][3][4][5][6] B7 transfection, however, often does not suffice to transfer immunogen...

show abstract

Effective anti‐metastatic melanoma vaccination with tumor cells transfected with MHC genes and/or infected with newcastle disease virus (NDV)

Cited by 35 publications

References 19 publications

Newcastle disease virus infection induces B7-1/B7-2-independent T-cell costimulatory activity in human melanoma cells

Newcastle disease virus infection induces B7-1/B7-2-independent T-cell costimulatory activity in human melanoma cells

Osteosarcoma cells as carriers to allow antitumor activity of canine oncolytic adenovirus in the presence of neutralizing antibodies

An effective strategy of human tumor vaccine modification by coupling bispecific costimulatory molecules

Contact Info

Product

Resources

About