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

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 zeta associated with CD3 and CD16 in tumour-associated T lymphocytes (TAL). Flow cytometric analysis revealed a significantly lower zeta 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+) zeta expression. The EBV status of the tumours did not correlate with zeta expression in the TAL. Immunohistochemical staining revealed zeta-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 zeta in TAL as a critical mechanism contributing specifically to the immune escape of EBV+ HRS cells.