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

Expression of T-cell antigens by Reed-Sternberg (RS) cells has not been detected in most studies of Hodgkin's disease (HD). The authors employed an improved method of fixation (paraformaldehyde-lysine-periodate), which sharply defined cell borders and revealed T-cell antigens on RS cells in 8 of 30 (27%) cases of HD. Antigen-specific staining was confirmed by immunoelectron microscopy. RS cells expressed T11 (8/8 cases), Leu-3 or T4 (4/8 cases), Leu-4 or T3 (3/8 cases), but not other T-cell specific antigens (Leu-1, T8, T6, 3A1). RS cells were negative for leukocyte common antigen (LCA/T200), in contrast to positive LCA/T200 staining of RS-like cells in T-cell lymphomas. RS cells in all HD cases were positive for Ki-1 and/or Leu-M1 antigens. The percentage of RS cells expressing T-cell antigens was less than 20% (2 cases), 20-50% (3 cases), or greater than 50% (3 cases). This percentage and the specific T-cell antigens expressed varied in tissues from different sites in each of 2 cases. Expression of T-cell antigens by RS cells was found in nodular sclerosis (6 of 20 cases) and mixed cellularity (2 of 5 cases) but not in lymphocyte predominance (2 cases), lymphocyte depletion (1 case), or unclassified types (2 cases). Two cases of nodular sclerosis contained areas of necrosis surrounded by sheets of lacunar cells (syncytial variant of NSHD). Two other cases were associated with cutaneous lymphoma. One of these cases was mixed cellularity HD, which appeared to be confined to the skin. In a second case, tumor cells of similar phenotype (T4+, Ki-1+) were found in skin and lymph nodes of a patient with coexistent mycosis fungoides and HD. These results are consistent with an origin of RS cells from T cells in some cases of nodular sclerosing and mixed cellularity HD. They also suggest that the same cell type, an activated helper T-cell, is involved in the pathogenesis of both skin lesions and lymphadenopathy of some patients with coexistent mycosis fungoides and HD.
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PMID:Expression of T-cell antigens on Reed-Sternberg cells in a subset of patients with nodular sclerosing and mixed cellularity Hodgkin's disease. 296 47

A novel cell line, KM-H2, was established from the pleural effusion of a patient with Hodgkin's disease of mixed cellular type. Multiple phenotypic studies were carried out with this cell line. Acid phosphatase and nonspecific esterase activities were detected. Rosette formation with T lymphocytes and the receptors for C3b and Fc portion of IgG were positive. Among the antigens tested with a total of 22 monoclonal antibodies defining hematopoietic cell subsets or lineages, Ki-1, Leu-M1, MCS1, HLA-DR, and OKT9 antigens were found to be positive. The other antigens reportedly specific for T cells, B cells, natural killer (NK) cells, monocytes, interdigitating reticulum (IR) cells and dendritic reticulum cells were negative. These phenotypic features were identical to those of the Sternberg-Reed (SR) and Hodgkin (H) cells in the fresh materials reported by other researchers. Moreover, the KM-H2 cells and the parental pleural effusion cells shared several structural chromosome anomalies. These findings indicated that the KM-H2 cells are derived from the SR and H cells. Molecular genetic analysis of the KM-H2 cells disclosed that the human immunoglobulin JH gene was rearranged but not the JK gene, and that the human T cell receptor beta chain gene was of the germline type. Based on these properties of the KM-H2 cells, Hodgkin's disease may be derived from a cell lineage other than T cell or B cell.
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PMID:Cytochemical, immunologic, chromosomal, and molecular genetic analysis of a novel cell line derived from Hodgkin's disease. 301 43

The monoclonal antibody Ki-1 reacts with Reed-Sternberg cells in Hodgkin's disease and with the tumour cells in a minority of large cell non-Hodgkin's lymphomas. This study describes the results of immunophenotypic and DNA analysis in 30 cases of non-Hodgkin's lymphoma, all of which expressed the Ki-1 antigen. The genotypic analysis has been undertaken using both immunoglobulin and T-cell receptor gene probes. Sixteen cases were shown by this method to be of monoclonal T-cell origin, six of B-cell origin, while in eight cases there was no evidence of either T- or B-cell lineage. This confirms previous immunohistological data indicating that non-Hodgkin's lymphomas which express the Ki-1 antigen may be of either T-cell or B-cell origin.
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PMID:Genotypic analysis of large cell lymphomas which express the Ki-1 antigen. 304 May 65

The Hodgkin-associated Ki-1 antigen was analyzed in different cell lines. In Hodgkin analogous L428 cells, biosynthetically labeled with radioactive amino acids, the Ki-1 antibody precipitated three glycoproteins with 90, 105, and 120 kDa, respectively. Surface-labeling revealed that the two larger components were membrane-associated forms of the Ki-1 antigen, although the 90-kDa molecule was shown in pulse-chase experiments to be the precursor of the 105- and 120-kDa forms. All three forms of the Ki-1 antigen possess a tunicamycin-sensitive 6-kDa N-linked carbohydrate moiety. O-Linked oligosaccharides could not be detected. Thus, the differences in m.w. are probably not due to glycosylation. The ionophore monensin prevented the appearance of the membrane-associated molecules, which demonstrated that they are assembled between the transcompartment of the Golgi complex and their insertion into the cell membrane. The 90-kDa precursor molecule cannot be generated by disulfide reduction from the two larger forms. After internal labeling with P-32, only the 105- and 120-kDa bands became visible, indicating that the Ki-1 molecule is phosphorylated after its processing into the two larger membrane-associated forms. Analysis of the Ki-1 antigens from other cell lines demonstrated that after external labeling of two other Hodgkin-derived cell lines, six Epstein-Barr virus lymphoblastoid cell lines and one human T leukemia virus I-positive T cell line, both the 105- and the 120-kDa membrane molecules could be detected, regardless of the presence or type of virus integrated.
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PMID:Biochemical characterization and biosynthesis of the Ki-1 antigen in Hodgkin-derived and virus-transformed human B and T lymphoid cell lines. 304 Aug 64

A monoclonal antibody was used for analysing the expression of the cellular myb (c-myb) protein in a variety of established human tumor cell lines and its decrease after induction of differentiation. Differentiated resting human T-cells and B-cells do not express detectable amounts of c-myb protein. However, upon mitogenic stimulation in vitro T-cells exhibit strong expression of the c-myb protein as demonstrated by immunocytochemical staining and indirect immunoprecipitation. In contrast to the transformed T-lymphoblastic cell line Molt-4, where c-myb protein is a nuclear antigen, it was found in proliferating normal T-cells almost exclusively distributed in the cytoplasm. Screening of a total of 70 fresh human malignant lymphomas by immunohistochemical staining indicates the presence of the c-myb protein primarily in non-Hodgkin's lymphomas with a large growth fraction, i.e. precursor cell-derived lymphoblastic lymphomas of B-cell type and T-cell type (9/10, 3/4, respectively) and anaplastic large cell Ki-1 lymphomas (5/9), which originate from activated lymphoid cells. The c-myb protein was located predominantly in the nucleus and in some cases additionally in the cytoplasm. The different subcellular locations suggest a dual functional role. While nuclear localisation is exhibited by transformed haematopoietic cells, cytoplasmic localisation appears to be characteristic for proliferating normal T-cells and points to a second property of the c-myb protein other than interaction with DNA.
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PMID:Nuclear and cytoplasmic distribution of cellular myb protein in human haematopoietic cells evidenced by monoclonal antibody. 306 Jul 91

The controversy in literature with regard to the origin of Hodgkin's and Reed-Sternberg cells persists, however only two conceptions seem to be plausible at present: the first is based on the relation to histiocytic elements, the second postulates lymphocytic precursors. The significance of surface-markers of these malignant cells in cryostat-sections and in cell-cultures and the relevance of their functional properties are discussed with respect to pathophysiology, clinical appearance, diagnosis and prognosis of Hodgkin's disease. The authors present two tendencies in the classification of malignant lymphomas based on the present knowledge achieved especially by monoclonal antibodies: the first includes aspects of integration between non Hodgkin's lymphomas and Hodgkin's disease, illustrated by the Ki-1-lymphoma, the second is related to separation of entities of the group of Hodgkin's lymphomas (for example the nodular paragranuloma). The aetiopathogenesis of Hodgkin's disease is considered as a causal trinity of virus infection, genetic determination and immunologic predisposition.
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PMID:[Hodgkin and Sternberg-Reed cells--cell origin, cell marker, cell function]. 306 1

Nodular lymphocyte predominance type of Hodgkin's disease can be distinguished from other subtypes of Hodgkin's disease on morphological and clinical grounds. Immunohistological studies on frozen tissue sections of seven cases of nodular lymphocyte predominance type of Hodgkin's disease (NLPHD) show differences in B cell, T cell, as well as dendritic cell population. NLPHD is confined to follicles which contain predominantly small lymphocytes, usually over 50% B cells and large numbers of B2+, anti-C3b+, anti-DRC+, and Ig- dendritic cells. The IgM+, IgD+, Leu8- B lymphocytes are of polyclonal origin. The T lymphocytes in these follicles are reactive with Leu7 in addition to T11, Leu1, T3, Leu3, and WT1. Leu7 is a monoclonal antibody reactive with natural killer cells, but also with a subpopulation of Leu3+ lymphocytes present in normal germinal centers. The population with this phenotype, not found in other types of Hodgkin's disease, appears to be greatly increased (up to 30%) in NLPHD. The so-called L&H type Sternberg-Reed (S-R) cells of NLPHD are transformed B cells, reactive with anti-B cell monoclonal antibodies which in some cases express detectable amounts of membrane and/or cytoplasmic immunoglobulin. Also, L&H type Sternberg-Reed cells in all cases stained for Ki-1 and Tac, and in three cases for LeuM1. Taken together, the findings indicate that NLPHD represents a proliferation of germinal center cells.
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PMID:Nodular lymphocyte predominance type of Hodgkin's disease is a germinal center lymphoma. 308 57

The lymphoid tissues from patients with infectious mononucleosis or, less frequently, with other reactive conditions may contain Reed-Sternberg (RS)-like cells. These tissues also contain cells resembling the lacunar cells or lymphocytic/histiocytic (L/H) variants, which are present in the lymphocyte-predominant type of Hodgkin's disease. The phenotype of these RS- and L/H-like cells was determined with a large panel of antibodies and lectins. The cells expressed sialylated Leu-M1, Con A, LN-2, and, less frequently, interleukin-1, S-100, and peanut agglutinin receptor. They reacted negatively with two markers for RS cells, Ki-1 and HeFi-1. These RS-like cells were consistently negative for T- and B-cell markers, including immunoglobulins. The markers of the RS-like cells are distinctly different from those in B-immunoblasts, but closely resemble those in interdigitating reticulum cells. It is concluded that interdigitating reticulum cells, when stimulated, can be transformed into lacunar-, L/H-, or RS-like cells.
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PMID:The H-RS-like cells in infectious mononucleosis are transformed interdigitating reticulum cells. 310 95

The past several years have seen major advances in the immunopathology of Hodgkin's disease, although the cell of origin remains unproven. Reed-Sternberg cells have been characterized with monoclonal antibodies and are found to consistently express panleukocytic antigen (T-200), HLA-DR antigens, and several activation-proliferation antigens (Tac, OKT-9, Ki-1). Reed-Sternberg cells also express a nonlineage-specific antigen defined by the antigranulocyte antibody Leu M-1. Lineage-specific B, T or monocyte-macrophage antigens are generally lacking. With the possible exception of the lymphocyte predominant form of the disease, Hodgkin's disease appears immunologically homogeneous. The possible origin of Reed-Sternberg cells by neoplastic transformation of antigen-presenting dendritic cells (interdigitating reticulum cells) appears to be an attractive albeit unproven hypothesis. Application of molecular biologic techniques in the future may yield definitive evidence as to the origin and nature of these enigmatic cells, and to the pathophysiology of the disease which they define.
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PMID:Immunopathology of Hodgkin's disease. 311 Jul 53

Three Hodgkin-derived cell lines (L428, L540, and CO) were studied for rearrangements and expression of immunoglobulin and T-cell receptor genes, and their genotype was compared to the phenotype. As far as the genotype is concerned, all 3 cell lines have characteristics of lymphoid cells; L428 of B, and L540 and CO of T-cell origin. L428 cells have one Ig heavy chain allele rearranged to C gamma and transcribed into RNA, while the second is deleted. Furthermore, L428 cells show an unusual immunoglobulin kappa light chain gene rearrangement involving deletion of the kappa constant gene in one allele, while the remaining kappa and lambda loci are in germline configuration. L540 and CO have, in contrast to L428 cells, the immunoglobulin genes in germline and T-cell receptor genes rearranged. The T-cell receptor beta and gamma genes are rearranged in both L540 and CO, whereas a rearrangement in the alpha locus was detected in L540 cells only. RNA of the size of functional beta chain transcripts was found in CO cells and of the size of functional alpha chain transcripts in L540 cells. All 3 cell lines are classified as immature lymphoid cells with respect to the limited expression of B- and T-cell antigens, respectively, and to the incomplete expression of their antigen receptor. The immaturity of lymphoid differentiation contrasts with the expression of activation antigens, i.e. Ki-1, Ki-24, HLA-DR, and IL-2 receptor. The immaturity of the cells excludes the possibility that the cells were activated along the physiological pathway, i.e. by interaction of the cell with antigen. The results obtained on the cell lines are in accordance with in vivo studies and suggest that Hodgkin and Sternberg-Reed cells are immature lymphoid cells which are activated by a still unknown mechanism.
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PMID:Phenotype versus immunoglobulin and T-cell receptor genotype of Hodgkin-derived cell lines: activation of immature lymphoid cells in Hodgkin's disease. 311 32


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