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Blood, 15 October 2008, Vol. 112, No. 8, pp. 3339-3347. Prepublished online as a Blood First Edition Paper on August 6, 2008; DOI 10.1182/blood-2008-01-134783. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-01-134783v1 112/8/3339    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lamprecht, B. Articles by Mathas, S. Search for Related Content PubMed PubMed Citation Articles by Lamprecht, B. Articles by Mathas, S. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Aberrant expression of the Th2 cytokine IL-21 in Hodgkin lymphoma cells regulates STAT3 signaling and attracts Treg cells via regulation of MIP-3 Björn Lamprecht1,2, Stephan Kreher1,2, Ioannis Anagnostopoulos3, Korinna Jöhrens3, Giovanni Monteleone4, Franziska Jundt1,2, Harald Stein3, Martin Janz1,2, Bernd Dörken1,2, and Stephan Mathas1,2 1 Max-Delbrück-Center for Molecular Medicine, Berlin, Germany; 2 Hematology, Oncology and Tumorimmunology, Charité, Medical University Berlin, Berlin, Germany; 3 Institute for Pathology, Charité, Medical University Berlin, Berlin, Germany; and 4 Dipartimento di Medicina Interna e Centro di Eccellenza per lo Studio delle Malattie Complesse e Multifattoriali, Università Tor Vergata, Rome, Italy The malignant Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (HL) are derived from mature B cells, but have lost a considerable part of the B cell–specific gene expression pattern. Consequences of such a lineage infidelity for lymphoma pathogenesis are currently not defined. Here, we report that HRS cells aberrantly express the common cytokine-receptor -chain (c) cytokine IL-21, which is usually restricted to a subset of CD4+ T cells, and the corresponding IL-21 receptor. We demonstrate that IL-21 activates STAT3 in HRS cells, up-regulates STAT3 target genes, and protects HRS cells from CD95 death receptor–induced apoptosis. Furthermore, IL-21 is involved in up-regulation of the CC chemokine macrophage-inflammatory protein-3 (MIP-3) in HRS cells. MIP-3 in turn attracts CCR6+CD4+CD25+FoxP3+CD127lo regulatory T cells toward HRS cells, which might favor their immune escape. Together, these data support the concept that aberrant expression of B lineage–inappropriate genes plays an important role for the biology of HL tumor cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Dien Bard, P. Gelebart, M. Anand, Z. Zak, S. A. Hegazy, H. M. Amin, and R. Lai IL-21 Contributes to JAK3/STAT3 Activation and Promotes Cell Growth in ALK-Positive Anaplastic Large Cell Lymphoma Am. J. Pathol., August 1, 2009; 175(2): 825 - 834. [Abstract] [Full Text] [PDF] D. Konforte, N. Simard, and C. J. Paige IL-21: An Executor of B Cell Fate J. Immunol., February 15, 2009; 182(4): 1781 - 1787. [Abstract] [Full Text] [PDF]

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