Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
Reed-Sternberg (RS) cells are natural hybridomas? (Meeting abstract).
Proc Annu Meet Am Soc Clin Oncol; 14:A328 1995. Unique Identifier : AIDSLINE ICDB/95613482 Sinkovics J; Cancer Inst., St. Joseph's Hosp., Tampa, FL 33607
Abstract:
Over 20 yr ago our team working at MD Anderson Hospital encountered 2 viral agents in Hodgkin's disease (HD): (1) an as yet unidentified retrovirus functioning as envelope donor to a defective mouse leukemia virus; and (2) a herpes virus that later turned out to be EBV. Patients with HD had antibodies to both of these agents. We construed a scenario of double infection of RS cells with these 2 agents proposing that the retrovirus is the primary pathogen infecting the mononuclear HD cell which is an antigen-presenting cell such as a follicular dendritic cell. These cells present intact antigens, ie, budding retroviral virions to reactive (oligoclonally expanding) or by-standing (naive) B and T cells. Due to the highly specialized interactions between antigen presenting cells and lymphocytes, not lymphocyte-mediated cytotoxic reaction but rather fusion between reactive or naive lymphocytes and retrovirally infected mononuclear HD cells takes place. Entirely similar reactions, ie, 'conjugate formations' or fusions between HIV-1-infected follicular dendritic cells and reactive lymphocytes are well documented (Cell 78:389, 1994). In HD the fusion product is what we recognize as the most versatile RS cell. It acquires EBV genomic sequences through fusion with EBV-carrier B cells. EBV certainly contributes to and modifies the pathogenicity of RS cells (BHRF-1 = imitating bcl-2; BNFL-1 = encoding LMP; Crit Rev Immun 11:33, 1991). We propose that RS cells are natural hybridomas. RS cells of nodular sclerosing HD are T cell hybridomas; RS cells of nodular lymphocyte predominant HD are B cell hybridomas; other clinical forms of HD are both B and T cell hybridomas or quadromas. Multinucleation of RS cells may not necessarily be due to endomitosis: when one nucleus is p53-positive and the other nucleus is p53-negative in the same RS cell (PNAS USA 90:2817, 1993), the cell fusion theory offers the best explanation for this discordance. When B cell Ig gene or T cell TCR gene rearrangements are detectable in RS cells (PNAS USA 91:9842;10962, 1994) oligoclonality of reactive B or T cells with which the mononuclear HD cell fused is an acceptable explanation. Animal models support the view that hybridomas can be formed naturally (Persp Biol Med 35:373, 1992).
Keywords: Antigen-Presenting Cells/*VIROLOGY Herpesvirus 4, Human/ISOLATION & PURIF Human *Hybridomas Reed-Sternberg Cells/*VIROLOGY Retroviridae/ISOLATION & PURIF ABSTRACT
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Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
