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Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation.

Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Research Abstract Details 

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  • Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Abstract Text:

    mechthild krauseMechthild Krause,marc schmitzMarc Schmitz,elfriede noessnerElfriede Noessner,petra s a skrablinPetra S A Skrablin,rebekka wehnerRebekka Wehner,ernst-peter rieberErnst-Peter Rieber,michael baumannMichael Baumann,

    PURPOSE: To evaluate whether immunotherapy based on adoptively transferred cytotoxic T-cells (CTL) can improve the antitumour efficacy of irradiation. MATERIAL AND METHODS: The experiments were performed using the human squamous cell carcinoma line UT-SCC-15, which expresses human leukocyte antigen (HLA)-A2. The UT-SCC-15 cell-mediated activation of JB4 CTL in terms of interferon (IFN)-gamma secretion and cytotoxic potential was determined by enzyme-linked immunosorbent assay and chromium release assay, the perforin content of JB4 cells by flow cytometry. In vivo, tumours were irradiated with 14 Gy. Subsequently, JB4 CTL were injected intra- and peritumourally. Volume doubling times were calculated as a marker of tumour growth delay. RESULTS: UT-SCC-15 tumour cells were well recognized by JB4 CTL in vitro, as indicated by profound IFN-gamma secretion and tumour cell lysis. This response was completely abrogated in the presence of an anti-HLA-A2 antibody. In vivo, adoptive transfer of JB4 CTL after irradiation did not delay tumour growth in comparison to irradiation alone. As a possible underlying mechanism, a loss of perforin content and cytolytic function of the CTL in the absence of interleukin (IL)- 2 or IL-15 was found in vitro. CONCLUSION: HLA-A2-alloreactive JB4 cells efficiently recognize and destroy UT-SCC-15 tumour cells in vitro. However, the intratumoural application of JB4 cells after irradiation does not enhance the in vivo effect of radiotherapy alone, which might be caused by the reduced cytotoxic potential of JB4 cells in the absence of IL-2 or IL-15. Thus, co-administration of these cytokines might improve the efficacy of combined irradiation and CTL treatment.

    Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Publishing Authors By Initials

    m krauseM Krause,m schmitzM Schmitz,e noessnerE Noessner,ps skrablinPS Skrablin,r wehnerR Wehner,ep rieberEP Rieber,m baumannM Baumann,

    For similar surgical procedures, operative: transplantation: transplantation, heterologous research abstracts see: surgical procedures, operative: transplantation: transplantation, heterologous research

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    Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: International journal of radiation biology

    VOLUME: 83

    Page Numbers: 827-36

    Journal Abbreviation: Int. J. Radiat. Biol.

    ISSN: 0955-3002

    DAY: 7

    MONTH: 03

    YEAR: 2008

    Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8809243

    Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Keywords Mesh Terms:

    KEYWORDS: Transplantation, Heterologous

    MESH TERMS: transplantation

    Chemical & Substance for Abstract: Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation. Information

    Substance Name: Interferon Type II

    Registry Number: 82115-62-6

    Grant and Affiliation Information for Adoptive transfer of cytotoxic T-cells for treatment of residual disease after irradiation.

    AFFILIATION: Department of Radiotherapy and Radiation Oncology, Medical Faculty Carl Gustav Carus, Technical University of Dresden, Germany. mechthild.krause@tu-dresden.de

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: Int J Radiat Biol

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