Amplification and expression of a decoy receptor for Fas ligand (DcR3) in virus (EBV or HTLV-I) associated lymphomas

The recently identified decoy receptor 3 (DcR3) binds to Fast and inhibits Fast-induced apoptosis, and is considered to play a role in the immune esca pe system of neoplastic cells. To examine the involvement of DcR3 in the im mune evasions of virus-associated lymphoma, we analyzed the amplification a nd expression of DcR3, using dot blot and in situ hybridization (ISH), in 4 5 cases, which included 17 cases with Epstein-Barr virus (EBV)-associated l ymphoma (seven pyothorax-associated B-cell lymphomas (PAL): ten natural kil ler lymphoma (NKL)), seven cases with adult T-cell leukemia lymphoma (ATLL) , 13 Hodgkins disease (eight EBV-associated cases; five non-EBV-associated cases), and eight control cases (three reactive lymphadenopathy; five non-E BV-associated-B-cell lymphoma). EBV-associated PAL and NKL exhibited DcR3 a mplification and expression in lymphoma cells. ATLL also showed DcR3 expres sion and amplification. The cases with DcR3 amplification showed DcR3 expre ssion; however, the expression was confined in the neoplastic cells, but no t in the reactive cells. In Hodgkin's disease (HD), DcR3 was expressed only in Hodgkin and Reed-Sternberg giant (H-RS) cells. However, DcR3 was not ex pressed or amplified in reactive lymphadenopathy. Non-EBV-associated B-cell lymphoma also rarely expressed DcR3, and showed no amplification except in two cases, in which rare expression was present. Our results suggest that EBV and HTLV-I probably use DcR3 to escape from the immune system during ly mphomagenesis, or virus-infected lymphoma cells with DcR3 expression might he selected in the multistep tumorigenesis. (C) 2000 Elsevier Science Irela nd Ltd. All rights reserved.