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Query: UMLS:C0019829 (Hodgkin's disease)
30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the histologic distribution of lymphocyte subpopulations in Hodgkin's disease. Involved tissues from 15 patients were stained by an indirect immunoperoxidase procedure for a variety of lymphocyte surface antigens using monoclonal antibodies. In most cases, there were more T cells than B cells, and Reed-Sternberg cells were found in T-cell rich areas. Except in lymphocyte-depleted Hodgkin's disease, helper-T antigen-positive (TH) cells greatly outnumbered cytotoxic-suppressor antigen-positive cells. Moreover, TH cells showed a preferential association with Reed-Sternberg cells. Lymphocytes surrounding Reed-Sternberg cells often expressed the transferrin receptor, a marker of cell activation. Our results do not support the hypothesis that the lymphocytes in Hodgkin's disease represent a cytotoxic T-cell response to neoplastic cells, except perhaps in the lymphocyte-depleted subtype.
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PMID:Immunohistochemical analysis of the distribution of lymphocyte subpopulations in Hodgkin's disease. 621 Apr 33

A panel of monoclonal antileucocyte antibodies was used in a study of Hodgkin's disease (HD) to explore the phenotypic characteristics of Sternberg-Reed and related cells (collectively termed HD cells). Cryostat preparations of 31 lymph nodes and 2 spleens were obtained from 30 patients with active HD. The histological diagnoses were: lymphocyte predominance (LP), 4 patients; nodular sclerosis (NS), 22; mixed cellularity (MC), 2; lymphocyte depletion (LD), 2. The monoclonal antibodies used were: OKT3, T11, Leu-1 (pan T cell specific); Leu-3A (T "helper" specific); Leu-2A, OKT8 (T "suppressor" specific); immunoglobulin (Ig) antibodies: anti kappa and lambda light chains, anti mu and delta heavy chains; B1 (anti B lymphocyte); CA2-11 (anti HLA-DR); OKM1, Mo-2 (anti myeloid/monocyte); OKT9 (anti transferrin receptor); Leu-7 (anti "NK" cell) and J5 (anti common ALL antigen). Reactions with peanut lectin (PNL) were also studied. The reactions were developed using a modified "ABC" immunoperoxidase technique. Specific attention was paid to the cell surface phenotype and anatomical localisation of HD cells in relation to surrounding T and B lymphocytes. HD cells formed distinct "rosettes" with T cells of "helper" phenotype although in 3 cases (1: LP, 2: NS) Leu-7 positive cells formed a prominent component of these interactions. In partially involved lymph node and spleen, HD cells were prominently distributed in a perifollicular distribution. In addition follicular mantle zones were frequently infiltrated by HD cells, the degree of ensuing destruction being related to the extent of lymph node effacement by HD. In 2 cases (1: NS, 1: LD) HD cells expressed clear, positive reactions with B1 although in neither of these cases nor in any other instance, was surface Ig expressed on the HD cell surface. The great majority of HD cells reacted positively with both OKT9 and, as previously reported, with anti HLA-DR antibody. In addition, HD cells demonstrated intense surface and cytoplasmic staining with PNL. HD cells were negative with all other antibodies. On the basis of these findings, no lineage specificity can confidently be attributed to the HD cell. However, the pattern of immunohistological reactions suggest that it is related to a cell of B follicular origins.
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PMID:Characteristics of Sternberg-Reed, and related cells in Hodgkin's disease: an immunohistological study. 637 Feb 86

Seven lymph nodes from patients with Hodgkin's disease were immunologically studied. Histologically these cases consisted of 3 lymphocyte predominance, 2 mixed cellularity, and 2 nodular sclerosis. Positive staining of mononuclear Hodgkin- and multinuclear Reed-Sternberg (RS) cells were obtained with anti-Ia like antigens and OKT9 (anti-transferrin receptor) monoclonal antibodies. No supportive data for discussing similarity of RS cells with ordinary histiocytes, B-lymphocytes or T-lymphocytes were obtained from the study of surface phenotype, although some analogy was present with histiocytes. Small lymphocytes around RS cells were helper/inducer T-lymphocytes, and the relationship between these T lymphocytes and RS cells was discussed.
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PMID:Immunologic characterization of Reed-Sternberg cells and other cell components in lymph nodes with Hodgkin's disease. 637 17

The cell lineage of suspensions prepared from 85 non-Hodgkin's lymphomas was investigated with a panel of 10 monoclonal antibodies and conventional surface marker techniques. Surface immunoglobulin, assessed with specific heteroantisera, proved to be the most useful characteristic and defined the clonal character and B-cell lineage of 63 specimens: almost all nodular lymphocytic (21 of 22) and diffuse lymphocytic (11 of 13) lymphomas, most diffuse histiocytic (29 of 33) and diffuse mixed (2 of 2) lymphomas, and a few nodular mixed (2 of 12) and nodular histiocytic (0 of 3) lymphomas. Monoclonal antibodies provided useful ancillary surface marker criteria. Thus, positivity with OKT1 (which detects both thymic and peripheral T cells) in the absence of reactivity with monoclonal antisera, which detect only peripheral T cells (OKT3, OKT4, OKT8, and OKT11), was seen only in diffuse lymphocytic lymphoma of B lineage. Ia-like antigen could be demonstrated in all B-cell lymphocytic lymphomas and most B-cell diffuse histiocytic lymphomas. Approximately one-half of diffuse histiocytic lymphomas also reacted with OKT9, which detects the transferrin receptor, while few lymph nodes involved by other conditions displayed this reactivity. Most diffuse histiocytic lymphomas and many non-Hodgkin's lymphomas of other subtypes reacted with OKT10, an antiserum that detects an antigen on replicating lymphoid cells. The lineage of approximately one-fourth of the lymphoma suspensions was not resolved conclusively: In most of these, T lymphocytes predominated with a normal proportion of inducer-helper (OKT4) and cytotoxic-suppressor (OKT8) cells. The inability to establish the clonal character of T-cell proliferation in cell suspensions remains an obstacle to completely defining the lineage of non-Hodgkin's lymphomas.
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PMID:Monoclonal antibody studies in non-Hodgkin's lymphoma. 682 84

We report a case of aggressive non-Hodgkin's lymphoma of the small cell type arising in the small intestine and having a natural killer cell phenotype. Immunophenotyping of frozen tissue sections revealed a lack of reactivity with the pan-T-cell markers CD3 and CD5, and no reaction with B-cell markers. Positive staining was obtained with antibodies to CD2, CD7, and CD56. Molecular studies were negative for clonal T gamma, T beta and immunoglobulin heavy-chain gene rearrangements. Natural-killer-cell-associated cytotoxin was demonstrated by positive staining with an antibody to perforin, a protein present in the granules of large granular lymphocytes. Despite its indolent histologic appearance, the aggressive nature of this neoplasm was suggested by the expression of the activation markers CD38 and CD71, and the nuclear proliferation marker Ki67, and confirmed clinically by its rapid recurrence with extensive involvement of the pelvic organs, resistance to chemotherapy, and the short survival of the patient. Distinct from many Asian cases, Epstein-Barr virus genome was not detectable in the tumor. This case emphasizes the importance of recognizing non-Hodgkin's lymphomas with a natural killer cell phenotype as a distinct entity, both biologically and clinically.
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PMID:Aggressive natural killer cell lymphoma of the small intestine. 767 62

A new cell line, SBH-1, with the morphologic, immunophenotypic, and karyotypic features consistent with those of Reed-Sternberg (RS) and Hodgkin (H) cells, has been established from the pleural effusion of a patient. The cytologic appearance of SBH-1 cells is characteristic of multinucleate RS and mononuclear H cells, all containing inclusion-like nucleoli. The SBH-1 cells express CD30, CD15, CD25, CD71, CD45, CD20, CD22, and bcl-2 protein and are negative for epithelial membrane antigen. Cytogenetic analysis showed multiple clonal abnormalities with breakpoints at 14q32, 6q21, and 11q23. The Ig heavy chain genes and both Ig light chain genes were rearranged in SBH-1 cells, whereas the bcl-2 gene was in germline configuration. Messages for the cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha, and transforming growth factor-beta and the cytokine receptors IL-2R, IL-4R, IL-6R, and IL-7R were detected by reverse transcription-polymerase chain reaction analysis. Xenotransplantation of SBH-1 cells into severe combined immunodeficient (SCID) mice led to local and disseminated tumor growth. The cytologic, histologic, and immunohistochemical features of SBH-1 cells in SCID mouse tumors were typical of RS and H cells. The SBH-1 cell line will be useful in the study of RS and H cell biology, inasmuch as it represents a cell line obtained from a previously untreated patient.
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PMID:SBH-1, a novel Reed-Sternberg-like cell line capable of inducing tumors in SCID mice: immunophenotypic, cytogenetic, and cytokine expression profiles. 774 44

Follicular dendritic cells (FDC) are restricted to the B-cell regions of secondary lymphoid tissue and to non-Hodgkin's lymphomas derived from the follicular center or the mantle zone. With their cytoplasmic ramifications they form a dense network which contains the B-lymphocytes. In situ, FDC are only detectable at the ultrastructural level or when stained with anti FDC-reagents. On the surface of their dendritic extensions they express transferrin receptors (CD71), the B-cell epitope CD20, class II antigens, the myelomonocytic molecule CD14, the glycoprotein gp50 (CD40), and several receptors for components of the complement system (CD11b, CD21, CD35). Subsequent to an antigen challenge, FDC trap and retain immune-complexes for a long period of time. In vitro FDC and neoplastic lymphocytes spontaneously form small cellular aggregates. This adhesion is mediated by the LFA-1-alpha/beta = ICAM-1, the VLA-4 = VCAM-1, and the ICAM-1 = C3bi- receptor ligand pathways on B-cells and on FDC, respectively. The loss of LFA-1- alpha/beta and ICAM-1 molecules may enable neoplastic lymphocytes to detach from FDC. The monoclonal B-cells now invade new compartments. In vitro, FDC have the capacity to activate resting B-cells and to save them from dying by apoptosis. Signals involved in this activation include cell-surface immunoglobulin and CD40. Immunocytochemistry and autoradiography with single cell suspensions of neoplastic B cells suggest that FDC also provide signals leading to the continued stimulation of lymphoma lymphocytes. During the early stage of HIV infection lymph nodes show an immense follicular hyperplasia, with a massive increase of the dendritic network of FDC. In the later stage of the disease, the continuous involution of the germinal centers is associated with a progressive destruction of FDC.
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PMID:Follicular dendritic cells in non-Hodgkin's lymphomas. 785 1

We recently characterized a novel putative intermediate-filament associated protein which is strongly expressed in the Reed-Sternberg cells of Hodgkin's disease. Therefore we named the protein 'restin', an acronym for Reed-Sternberg cell intermediate filament-associated protein. The protein is also expressed in anaplastic large cell lymphoma or Ki-1 lymphoma, a non-Hodgkin's lymphoma phenotypically related to Hodgkin's disease. Although the functions of restin are not yet fully elucidated, transfection experiments demonstrate that overexpression of the protein increases cell growth by a mechanism which may involve upregulation of the transferrin receptor. Hence, restin may contribute to neoplastic transformation in Hodgkin's disease and anaplastic large cell lymphoma. Study of the mechanisms leading to restin overexpression may provide important data on the etiology of Hodgkin's disease and its relation to anaplastic large cell lymphoma.
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PMID:Restin in Hodgkin's disease and anaplastic large cell lymphoma. 816 33

High-grade B-cell-type non-Hodgkin's lymphomas are observed in 5% to 8% of patients positive for the human immunodeficiency virus. Nearly all cases belong to one of the three major histologic types: centroblastic or large noncleaved cell, immunoblastic and Burkitt's lymphoma, or small noncleaved cell. Some cases that are polymorphic are termed high-grade B-cell, not otherwise specified (NOS). The authors determined the immunophenotype of each histologic category of acquired immunodeficiency syndrome (AIDS)-related non-Hodgkins' lymphoma and sought a relationship with the presence of the Epstein-Barr virus (EBV). B-cell differentiation antigens, activation marker expression (human leukocyte antigen-DR, CD10, CD19, CD20, CD21, CD22, CD23, CD25, CD30, CD38), and epithelial membrane antigen were analyzed. The clonality was determined by the detection of cytoplasmic immunoglobulin, surface immunoglobulin, and the analysis of joining region (JH) immunoglobulin gene configuration by Southern blot. Epstein-Barr virus was detected either by Southern blot analysis using BamHI W probe fragment or by in situ hybridization with EBV-encoded RNA transcripts-1 specific probe. The immunophenotypic and genotypic results were compared with the morphology results and with the presence or absence of EBV. Burkitt's lymphomas were associated with EBV in 50% of cases, were monoclonal, and expressed mostly immunoglobulin (Ig) MK, CD10, CD19, CD20, CD22, and CD38. This immunophenotypic profile closely resembled those of the centroblastic cases (large noncleaved cell), in which EBV was absent. Epstein-Barr virus was associated with 90% of immunoblastic cases, and only CD10, CD20, and CD38 were expressed. CD71 was expressed in all categories of non-Hodgkin's lymphoma, and CD21 and CD23 were rarely expressed. Two cases of immunoblastic lymphoma and one case of high-grade B-NOS were polyclonal regarding JH rearrangement, but EBV tested with 1.9-Kb Xhol fragment was clonal. No significant immunophenotypic changes were noted in relation to the presence of EBV. Such studies comparing morphology, immunophenotype, and genotype could help classify and better understand the pathogenesis of AIDS-related non-Hodgkin's lymphoma.
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PMID:Immunophenotypic and genotypic analysis of acquired immunodeficiency syndrome-related non-Hodgkin's lymphomas. Correlation with histologic features in 36 cases. French Study Group of Pathology for HIV-Associated Tumors. 820 68

We measured the soluble (s) receptors CD23, CD8, CD4, interleukin-2 receptor (IL-2R, CD25), and transferrin receptor (TfR, CD71), in normal serum and in patients with chronic lymphocytic leukemia (CLL) and evaluated them in relation to clinical and biological parameters of the disease, as well as serum immunoglobulin E (IgE). Compared to 31 normal individuals, 42 CLL patients had increased levels of sCD23 (98.4 +/- 127.7 versus 0.9 +/- 0.3 U/ml, p < 0.001), sIL-2R (6080 +/- 7030 versus 1420 +/- 640 pg/ml, p < 0.001), sTfR (12,100 +/- 11,250 versus 5000 +/- 1050 ng/ml, p < 0.001), and sCD8 (510 +/- 191 versus 234 +/- 89 U/ml, p < 0.001), but normal sCD4 levels. Mean sCD23 levels remained normal in patients with non-Hodgkin's lymphoma (other than small lymphocytic), Hodgkin's disease, hairy cell leukemia, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML), multiple myeloma, or solid tumors. Advancing Rai clinical stage was associated with a progressive elevation of sCD23 (p < 0.001), while sCD8 (p < 0.05), sIL-2R (p < 0.001), and sTfR (p < 0.005) were highest in stage 2 patients. Discriminant analysis confirmed the value of soluble receptor determinations in the clinical evaluation of CLL patients. sCD23 correlated with sIL-2R (p < 0.001) and sTfR (p < 0.05) but not with sCD4 or sCD8, and displayed an inverse relationship with serum IgE (NS) and total gamma-globulin (p < 0.05). sIL-2R correlated with sCD23 (p < 0.001), sTfR (p < 0.001), sCD4 (p < 0.01), and sCD8 (p < 0.01). The lymphocyte count correlated with serum lactate dehydrogenase (LDH) (p < 0.05), sCD23 (p < 0.001) and sIL-2R (p < 0.01) but not sTfR, sCD8, or sCD4. Chemotherapy produced consistent reductions of sCD23 levels in two responding patients. We conclude that: (i) sCD23 is considerably elevated in CLL, correlates with the tumor mass and clinical stage, and could be helpful in monitoring these patients; and (ii) sIL-2R, sCD8, and sTfR levels are less specifically increased and could be influenced by other factors such as immune activation and erythropoiesis.
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PMID:Soluble CD23 and other receptors (CD4, CD8, CD25, CD71) in serum of patients with chronic lymphocytic leukemia. 825 2


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