Reed-Sternberg cell
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Etiology
- Hodgkin's disease,
- small numbers in several types of non-Hodgkin's lymphoma.
* currently thought that Hodgkin's disease may be a heterogenous disease derived from subpopulations of activated B-cells. activated T-cells & dendritic cells[2]
Pathology
- usually derived from B-cells[2]
- multinucleated or bilobed nuclei 'Owl eyes'
- eosinophilic inclusion-like nucleoli
- give tissue a 'starry sky' or 'moth-eaten' appearance
Immunophenotype
- distinguished by their lack of leukocyte antigen expression characteristic of T-cells & B-cells.
- expression of CD25 (low-affinity IL-2 receptor) & CD71 (transferrin receptor) which are also expressed on activated B-cells, T-cells & NK-cells, & CD13 expressed on myeloid cells
- they also express MHC class II antigens & epithelial membrane antigen.
- Reed-Sternberg cells of the lymphocyte-predominant form of Hodgkin's disease express CD45R, whereas all other Reed-Sternberg cells are negative, a feature of dendritic cells.
- two unique antigens are expressed on the Reed-Sternberg cell:
- CD15 the Lewis X blood group antigen, which functions as an adhesion receptor
- not expressed on Reed-Sternberg cells of the lymphocyte-predominant form of Hodgkin's disease
- CD30 or Ki-1
- CD30 is also expressed on some activated B-cells, activated T-cells, dendritic cells, Epstein-Barr virus-transformed cell lines, Ki-1 large cell anaplastic lymphoma.
- CD15 the Lewis X blood group antigen, which functions as an adhesion receptor
Genetics
- immunoglobulin gene rearrangement have been demonstrated in some specimens of Reed-Sternberg cells (usually lymphocyte-predominant Hodgkin's) & T-cell receptor beta chain rearrangements have been demonstrated in others
- gene rearrangements in T-cell receptor gamma chains have been observed
- in-situ hybridization studies have identified the Epstein-Barr virus genome in Reed-Sternberg cells in 30% of Hodgkin's cases