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Modulation of interleukin‐6 expression in Hodgkin and Reed–Sternberg cells by Epstein–Barr virus
Author(s) -
Herbst Hermann,
Samol Jens,
Foss HansDieter,
Raff Thorsten,
Niedobitek Gerald
Publication year - 1997
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199707)182:3<299::aid-path856>3.0.co;2-8
Subject(s) - epstein–barr virus , virus , reed–sternberg cell , biology , in situ hybridization , herpesviridae , cancer research , gene expression , microbiology and biotechnology , virology , immunology , gene , lymphoma , viral disease , genetics , hodgkin lymphoma
Variable proportions of Hodgkin's disease (HD) cases are associated with the Epstein–Barr virus (EBV), but the role of EBV in HD is not entirely clear. Hodgkin and Reed–Sternberg (HRS) cells of EBV‐associated HD are characterized by expression of the EBV gene product LMP1. In other cellular environments, LMP1 has been shown to induce interleukin (IL)‐6. In this study, 105 HD cases were tested for differences in IL‐6 expression among LMP1‐positive and ‐negative cases. Isotopic in situ hybridization and correlation with the presence of EBV gene products revealed significantly higher proportions of cases with IL‐6‐expressing tumour cells in LMP1‐positive (31 of 37, 84 per cent) as compared with LMP1‐negative HD cases (35 of 68, 51 per cent). Thus, although not exclusive to EBV‐positive HRS cells, IL‐6 expression appears to be upregulated in EBV‐associated HD. IL‐6 receptor (CD126) expression was tested by in situ hybridization and found in a broad spectrum of cell types, regularly including HRS cells. Superinduction of IL‐6 expression may be among the mechanisms by which EBV confers a growth advantage on virus‐infected HRS cells and by which the virus may contribute to the morphological and clinical peculiarities of HD. © 1997 John Wiley & Sons, Ltd.