Expression of the signal transduction molecule ζ in peripheral and tumour‐associated lymphocytes in Hodgkin's disease in relation to the Epstein–Barr virus status of the tumour cells

Abstract

Summary. We investigated whether the described immune evasion of Epstein–Barr virus (EBV)‐infected malignant Hodgkin and Reed‐Sternberg (HRS) cells in Hodgkin's disease (HD) is paralleled by a disturbed expression of the signal transduction molecule ζ associated with CD3 and CD16 in tumour‐associated T lymphocytes (TAL). Flow cytometric analysis revealed a significantly lower ζ expression in CD3+/4+, CD3+/8+ and CD16+ patient peripheral blood lymphocytes (PBL; n = 10) compared with normal donor PBLs (n = 11). When patient PBLs were compared with the corresponding TAL, the latter showed a significantly higher (CD3+/4+) or equal (CD3+/8+) ζ expression. The EBV status of the tumours did not correlate with ζ expression in the TAL. Immunohistochemical staining revealed ζ‐positive lymphocytes among the adjacent bystander cells of the HRS cells in all analysed tumours (n = 8), irrespective of tumour EBV status. In conclusion, these results do not support downregulation of ζ in TAL as a critical mechanism contributing specifically to the immune escape of EBV+ HRS cells.