B- and T-lymphocytes in Hodgkin's disease. An immunohistochemical study utilizing heterologous and monoclonal antibodies (original) (raw)
Related papers
Cancer, 1989
The authors analyzed 50 cases of Hodgkin's disease (HD) with a panel of antibodies which detect B-cell and T-cell specific markers and activation antigens using a sensitive immunocytochemical technique and paraformaldehyde-lysine-periodate (PLP) fiued-frozen tissues. In 60% of cases either T-cell or B-cell specific antigens were detected on Reed-Sternberg (RS) cells. Most T-cell cases were of nodular sclerosing (NS) and mixed cellularity (MC) type (6540 and 30%, respectively) and most B-cell cases were either of NS or lymphocyte predominant (LP) type (55% and 458, respectively). Leukocyte common antigen (LCA) was usually negative on RS cells in NS, but was present in approximately 50% of the cases of MC and LP types. Almost all cases were positive for the CD30 antigen (Ki-I). Most cases were also positive for CD15 (LeuM1) with the exception of the LP type. Activation antigens (Ia, CD25, T9) were expressed in a high proportion of cases regardless of subtype. The results suggest that most cases of H D are histogenetically derived from activated T-cells or B-cells.
…, 1984
An immunohistological study of the cellular constituents of Hodgkin's disease using a monoclonal antibody panel Cryostat sections of lymphoid tissue from 4 cases of Hodgkin's disease were analysed by immunoperoxidase staining using a panel of monoclonal antibodies which included reagents reactive with T cells and their subsets, B cells, HLA-DR, Ig, dendritic reticulum cells and C3b receptor. A wide spectrum of immunohistological patterns was observed ranging from cases in which T cells were numerous (B cells being absent or present in only small numbers) to cases in which very prominent B cell follicles were present. These follicles contained a meshwork of dendritic reticulum cells and were composed of polyclonal B cells (as assessed by light chain expression). T cells were present in small numbers within these B cell follicles, often clustered in a thin rim around individual ReedSternberg and Hodgkin's cells. All B cell-rich cases were examples of lymphocyte predominant Hodgkin's disease. Assessment of the T cell helper/suppressor ratios was hindered by the fact that both anti-helper antibodies (OKT4 and anti-leu 3a) reacted with macrophages. However the majority of cases appeared to contain a normal excess of T helper cells. HLA-DR was strongly expressed in T cell rich areas, on Reed-Sternberg and Hodgkin's cells, on vascular endothelium and on numerous infiltrating cells in the fibrous tissue areas in cases of nodular sclerosing disease. Reed-Sternberg and Hodgkin's cells were not labelled by either anti-fibronectin or by antibodies reactive with dendritic reticulum cells (anti-Qb receptor and antibody R4/23).
Immunogenotyping in Hodgkin's disease
Hematological Oncology, 1988
This review presents and discusses the immunogenotypic findings in 1 12 cases of Hodgkin's disease (HD) and eight Hodgkin's cell lines. Clonal rearrangements of the T cell receptor y andachain, as well as immunoglobulin heavy and light chain genes, are detected in the majority of nodular sclerosis and lymphocytic depletion subtypes. Together with the recent immunophenotypic data, these findings are in favour of the view that HD is a disease of activated lymphoid cells.. Further investigations will be necessary to characterize the morphology and immunophenotype of the clonally rearranged cell population which seems not to be confined to the Sternberg-Reed and Hodgkin cell in every case. Prospective clinical studies including the genotype of HD cases have to be done in order to address the question of whether or not distinctive immunogenotypic profiles correlate with the clinical course of this lymphoproliferative disorder.
Coexpression of CD15 and CD20 by Reed-Sternberg cells in Hodgkin's disease
PubMed, 1991
The immunophenotype of the Reed-Sternberg cells in Hodgkin's disease is heterogeneous among different cases; this heterogeneity has contributed to the continuing uncertainty regarding the normal counterpart of the Reed-Sternberg cell. In this study, the authors demonstrate coexpression of the B-cell marker, CD20, and the granulocyte associated antigen, CD15, by Reed-Sternberg cells in three of 20 cases of nodular sclerosis and mixed cellularity Hodgkin's disease using a double-labelling technique in one case and staining of serial sections in three cases. Additionally, the authors found that expression of CD20 occurred more often in tumors with a monomorphous proliferation of mononuclear and binucleate Hodgkin's and Reed-Sternberg cells, without numerous eosinophils or polymorphonuclear neutrophils. In contrast, expression of CD15 by Reed-Sternberg cells was associated with a greater granulocyte infiltrate. The presence or absence of fibrosis, plasma cells, and histiocytes did not correlate with antigen expression. These results suggest that there may be a continuum of antigen expression by Reed-Sternberg cells, with some cells expressing CD20, some CD15, and others expressing both antigens; cells coexpressing both CD15 and CD20 may represent an unstable intermediate in the process of antigen switching. The possibility that antigen expression by the neoplastic cells in a given case may modulate depending on the background infiltrate could explain the heterogeneity of immunophenotype among cases of Hodgkin's disease.
Evidence that Hodgkin and Reed-Sternberg cells in Hodgkin disease do not represent cell fusions
Blood, 2001
In most cases, Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin disease (HD) carry rearranged immunoglobulin (Ig) genes and thus derive from B cells. In rare cases, HRS cells originate from T cells. However, based on the unusual immunophenotype of HRS cells, often showing coexpression of markers typical for different hematopoetic lineages, and the regular detection of numerical chromosomal abnormalities, it has been speculated that HRS cells might represent cell fusions. Five cases of HD with 2 rearranged IgH alleles were analyzed for the presence of additional IgH alleles in germline configuration as a potential footprint of a cell fusion between a B and a non-B cell. Similarly, one case of T-cell-derived HD with biallelic T-cell receptor  (TCR) rearrangements was studied for the presence of unrearranged TCR alleles. In none of the 6 cases was evidence for additional IgH (or TCR) alleles obtained, strongly arguing against a role of cell fusion in HRS cell generation. (Blood. 2001;97:818-821)
The pathology of Hodgkin's disease: What's new?
Seminars in Radiation Oncology, 1996
From the viewpoint of the pathologist, there are three major issues concerning Hodgkin's disease (HD) that must be addressed. First is making the correct diagnosis; second is identifying any pathological features that may be of prognostic importance; and third is defining the identity of the neoplastic cell. Since Hodgkin's disease (HD) was first described, the origin of the Reed-Sternberg cell and the pathogenesis of HD have remained elusive. Recently developed techniques have allowed investigators to analyze the immunophenotype and genotype of Reed-Sternberg cells. The results of these studies include recognition that, in many cases, Reed-Sternberg cells are of lymphoid origin. Thus, although in most cases of HD the diagnosis is straightforward on routinely stained sections, the conceptual dividing line between HD and non-Hodgkin's lymphoma is not as sharp as it once seemed. Occasionally, there is difficulty in distinguishing between HD and non-Hodgkin's lymphoma. Nevertheless, fundamental differences in the clinical features, histology, immunophenotype, and genotype between non-Hodgkin's lymphoma and HD remain. The impact of histological features on prognosis are controversial, largely because of the excellent prognosis of most cases of HD.
Cancer, 1988
The authors have reviewed their experience using the antigranulocyte marker, anti-Leu-M1, in combination with the antileukocyte marker, PD7/26, applied to paraffin sections of malignant lymphomas difficult to subclassify using morphologic criteria. The study group consisted of 73 lymphomas; 53 cases of Hodgkin's disease and 20 cases of non-Hodgkin's lymphoma. Leu-M1 was expressed by the Reed-Sternberg and Hodgkin's cells in 33 (62%) of the cases of Hodgkin's disease. The Reed-Sternberg and lymphocytic and histiocytic (L&H) cells in four cases of lymphocyte-predominant Hodgkin's disease were Leu-M1 negative. The Reed-Sternberg cells and L&H cells expressed leukocyte common antigen, utilizing the monoclonal antibody PD7/26, in seven (13%) of the 53 cases including the four cases of lymphocyte-predominant subtype (three nodular, one diffuse). The Reed-Sternberg-like cells in four (20%) of the cases of non-Hodgkin's lymphoma were stained by anti-Leu-M1 whereas, in 12 cases (60%) these cells were stained by PD7/26. The combination of anti-Leu-M1 and PD7/26 provided more useful information than that provided by anti-Leu-M1 alone by providing immunologic support for the diagnosis of lymphocyte-predominant Hodgkin's disease and by identifying cases which stained with neither antibody. The authors interpret the immunologic findings in the latter cases as equivocal. These studies were most helpful in cases with many atypical cells and provided unequivocal support for the diagnosis of Hodgkin's disease in six of 11 cases of the "syncytial variant," a form of the nodular sclerosing type characterized by cohesive aggregates of Reed-Sternberg cells and lacunar variants, not uncommonly misdiagnosed using only morphologic criteria.
Proceedings of the National Academy of Sciences, 1994
Hodgkin disease (HD) is characterized by a small number of putative malignant cells [Hodgkin and Reed-Sternberg (HRS) cells] among a background of lymphocytes and histiocytes. The lineage of HRS cells is still elusive and a clonal origin of these rare cells has not formally been demonstrated. We isolated HRS cells by micromanipulation from histological sections of three cases of Hodgkin lymphoma (each representing a distinct subtype of the disease) and analyzed individual cells for immunoglobulin variable (V) gene rearrangements by PCR. In each of the three cases a single heavy-chain V (VH) (and in one case, in addition, a kappa light-chain) gene rearrangement was amplified from the HRS cells, identifying these cells as members of a single clone. A potentially functional VH rearrangement was obtained from a case of nodular sclerosis HD. Somatic mutations and intraclonal diversity in the VH genes indicate a germinal center B-cell origin of the HRS cells in a case of lymphocyte-predom...