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  • CELL-LINES  (1)
  • EFFECTOR FUNCTIONS  (1)
  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; CELL ; Germany ; human ; PATHWAY ; SYSTEM ; GENE ; GENES ; PROTEIN ; LINES ; ACTIVATION ; MARKER ; T cell ; T cell activation ; T cells ; T-CELL ; T-CELLS ; BINDING ; CELL-LINES ; SIGNAL ; virus ; IDENTIFICATION ; NUMBER ; CELL-LINE ; LINE ; HUMAN-IMMUNODEFICIENCY-VIRUS ; representational difference analysis ; GENE-PRODUCT ; SUBSET ; PRODUCTS ; HIV ; IMMUNODEFICIENCY VIRUS ; NUCLEOCYTOPLASMIC TRANSPORT ; TAP ; 60S RIBOSOMAL-SUBUNITS ; CD83 ; CRM1 ; IMMUNODEFICIENCY-VIRUS REV ; LEPTOMYCIN B ; RAN ; RECEPTOR CRM1 ; RNA export
    Abstract: In metazoans, the nuclear export of bulk mRNAs is mediated by the export receptor TAP, together with its binding partner p15. A number of viral mRNAs, including the unspliced and partially spliced mRNA species of the human immunodeficiency virus (HIV), however, use an alternative export route via the importin beta-related export receptor CRM1. This raises the question of whether a subset of cellular mRNAs might be exported by CRM1 as well. To identify such mRNAs, we performed a systematic screen in different cell lines, using representational difference analyses of cDNA (cDNA-RDA). In HeLa and Cl-4 cells no cellular transcripts could be identified as exported via CRM1. In contrast, we found a number of CRM1-dependent mRNAs in Jurkat T cells, most of which are induced during a T cell response. One of the identified gene products, the dendritic cell marker CD83, was analyzed in detail. CD83 expression depends on a functional CRM1 pathway in activated Jurkat T cells as well as in a heterologous expression system, independent of activation. Our results point to an important role of the CRM1-dependent export pathway for the expression of CD83 and other genes under conditions of T cell activation. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16580684
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  • 2
    Keywords: IMMUNE-RESPONSES ; tumor-infiltrating lymphocytes ; MELANOMA PATIENTS ; ANTITUMOR IMMUNITY ; REGULATORY T-CELLS ; CLINICAL-RESPONSES ; EFFECTOR FUNCTIONS ; BONE-MARROW MICROENVIRONMENT ; PREDICT RESPONSE ; IMMUNOLOGICAL ASPECTS
    Abstract: Breast cancer is a systemic disease with a primarily local component. Besides surgical resection and irradiation of the locoregional tumor setting, central therapeutic aim is the elimination of disseminated micrometastatic tumor cells using cytostatic and/or hormonal treatment. Nevertheless, in the course of time a majority of patients suffer from systemic recurrence in the form of distant metastases. Intriguingly, in this connection, intratumoral cytotoxic T lymphocytes might serve as independent predictors of treatment efficacy and clinical outcome. Loss of immune balance (tumor dormancy) during intensive cross talk between T cells and tumor cells in the bone marrow microenvironment is suggested one reason for distant metastatic relapse. In this clinical context, further supportive therapies become increasingly attractive, taking immunological features of breast cancer cells into special account. The present review aims to dissect bone marrow-derived cellular antitumor immune responses and translational immunologic treatment options regarding their actual relevance to patients' clinical benefit and their future directions in breast cancer management.
    Type of Publication: Journal article published
    PubMed ID: 24337953
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