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      Hodgkin/Reed-Sternberg cells induce fibroblasts to secrete eotaxin, a potent chemoattractant for T cells and eosinophils.

      Blood
      Cells, Cultured, Chemokine CCL11, Chemokines, CC, Chemotactic Factors, Eosinophil, genetics, Chemotaxis, Leukocyte, Cytokines, secretion, Enzyme-Linked Immunosorbent Assay, Fibroblasts, cytology, pathology, physiology, Gene Expression Regulation, HeLa Cells, Hodgkin Disease, Humans, In Situ Hybridization, Lymph Nodes, RNA, Messenger, Reed-Sternberg Cells, Skin, Th2 Cells, Transcription, Genetic, Tumor Cells, Cultured

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          Abstract

          Hodgkin's disease is histopathologically characterized by the relative scarcity of neoplastic Hodgkin and Reed-Sternberg cells and for yet unknown reasons by an abundant reactive background of T lymphocytes and often eosinophils. Eotaxin is a CC-chemokine attracting eosinophils and T helper 2 (Th2) cells in allergic inflammation. We now report that eotaxin is strongly expressed in fibroblasts of Hodgkin's disease tissues, whereas Hodgkin/Reed-Sternberg cells do not express this chemokine. In tissue culture, Hodgkin's disease tumor cells induce eotaxin expression in cocultured dermal fibroblasts in a concentration leading to a specific chemotactic response of a Th2 cell clone. Production of tumor necrosis factor-alpha (TNF-alpha) by Hodgkin/Reed-Sternberg cells appears to be responsible for this induction, because blocking of TNF-alpha by neutralizing antibodies prevented fibroblast eotaxin expression. Our data suggest that eotaxin is involved in the pathobiology of Hodgkin's disease by contributing to eosinophil and T-lymphocyte recruitment.

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