Evidence of abortive plasma cell differentiation in Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma.
Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) show genotypic features of germinal centre-derived B-cells in most cases. Nevertheless, these cells typically lack expression of B-cell antigens. Previous studies have suggested that plasma cell differentiation may occur in HRS cells and that this may account for the down-regulation of B-cell antigens. However, these results are controversial. We have addressed this question using immunohistochemistry and a panel of antibodies directed against antigens which are differentially expressed during terminal B-cell differentiation. Pax-5, a transcription factor required for B-lineage commitment, and IRF4/Mum1, which is physiologically expressed in germinal centre cells and plasma cells, were consistently detectable in HRS cells. Bcl-6, a transcription factor expressed in germinal centre B-cells, was present in HRS cells of approximately 25% of cHL cases. Expression of the B-lymphocyte-induced maturation protein-1 (Blimp-1), a key regulator of plasma cell differentiation, was observed in HRS cells of 23% of cHL cases. In these cases, Blimp-1 expression was restricted to a small proportion of HRS cells. HRS cells were consistently negative for the plasma cell marker CD138. These results suggest that plasma cell differentiation may be initiated in a small subset of HRS cells but remains abortive. Thus, terminal differentiation is unlikely to explain the lack of B-cell antigen expression in HRS cells.
Buettner
Maike
M
Institute for Pathology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, Friedrich-Alexander-University, Erlangen, Germany. maike.buettner@patho.imed.uni-erlangen.de
Greiner
Axel
A
Avramidou
Athanasia
A
Jäck
Hans-Martin
HM
Niedobitek
Gerald
G
D002471:Cell Transformation, Neoplastic / Q000378:metabolism* / Q000473:pathology; D015973:Gene Expression Regulation, Leukemic; D006689:Hodgkin Disease / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D009363:Neoplasm Proteins / Q000096:biosynthesis*; D010950:Plasma Cells / Q000378:metabolism* / Q000473:pathology; D011509:Proteoglycans / Q000096:biosynthesis; D016539:Reed-Sternberg Cells / Q000378:metabolism* / Q000473:pathology; D053668:Syndecan-1; D053667:Syndecans; D014157:Transcription Factors / Q000096:biosynthesis*
D008562:Membrane Glycoproteins; D009363:Neoplasm Proteins; D011509:Proteoglycans; C508241:SDC1 protein, human; D053668:Syndecan-1; D053667:Syndecans; D014157:Transcription Factors