title: Amplification and expression of a decoy receptor for fas ligand (DcR3) in virus (EBV or HTLV-I) associated lymphomas.
abstract: The recently identified decoy receptor 3 (DcR3) binds to FasL and inhibits FasL-induced apoptosis, and is considered to play a role in the immune escape system of neoplastic cells. To examine the involvement of DcR3 in the immune evasions of virus-associated lymphoma, we analyzed the amplification and expression of DcR3, using dot blot and in situ hybridization (ISH), in 45 cases, which included 17 cases with Epstein-Barr virus (EBV)-associated lymphoma (seven pyothorax-associated B-cell lymphomas (PAL); ten natural killer lymphoma (NKL)), seven cases with adult T-cell leukemia lymphoma (ATLL), 13 Hodgkin's disease (eight EBV-associated cases; five non-EBV-associated cases), and eight control cases (three reactive lymphadenopathy; five non-EBV-associated-B-cell lymphoma). EBV-associated PAL and NKL exhibited DcR3 amplification and expression in lymphoma cells. ATLL also showed DcR3 expression and amplification. The cases with DcR3 amplification showed DcR3 expression; however, the expression was confined in the neoplastic cells, but not 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 expressed 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 lymphomagenesis, or virus-infected lymphoma cells with DcR3 expression might be selected in the multistep tumorigenesis.
authors.affiliation: Department of Pathology, School of Medicine, Fukuoka University, Nanakuma 7-45-1, Jonan-ku, 814-0180, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ohshima
authors.forename: S
authors.initials: S
authors.lastname: Haraoka
authors.forename: M
authors.initials: M
authors.lastname: Sugihara
authors.forename: J
authors.initials: J
authors.lastname: Suzumiya
authors.forename: C
authors.initials: C
authors.lastname: Kawasaki
authors.forename: M
authors.initials: M
authors.lastname: Kanda
authors.forename: M
authors.initials: M
authors.lastname: Kikuchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002051:Burkitt Lymphoma / Q000235:genetics* / Q000473:pathology / Q000821:virology; D002648:Child; D053222:Fas Ligand Protein; D005260:Female; D005784:Gene Amplification; D015972:Gene Expression Regulation, Neoplastic; D005838:Genotype; D004854:Herpesvirus 4, Human / Q000235:genetics; D006689:Hodgkin Disease / Q000235:genetics / Q000473:pathology; D006801:Humans; D017403:In Situ Hybridization; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000235:genetics* / Q000473:pathology / Q000821:virology; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods; D010641:Phenotype; D012334:RNA, Neoplasm / Q000235:genetics / Q000378:metabolism; D012367:RNA, Viral / Q000235:genetics / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics* / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor; D053323:Receptors, Tumor Necrosis Factor, Member 6b
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D012334:RNA, Neoplasm; D012367:RNA, Viral; D011956:Receptors, Cell Surface; D018124:Receptors, Tumor Necrosis Factor; D053323:Receptors, Tumor Necrosis Factor, Member 6b; C505911:TNFRSF6B protein, human