Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes the antigenic profile of the proliferating cells of pulmonary histiocytosis X (HX) in a patient treated with chemotherapy for Hodgkin's lymphoma; the association of pulmonary HX and Hodgkin's disease has rarely been described in the literature. The histopathological diagnosis of HX was confirmed with the aid of monoclonal antibodies (mAbs) to CD4, CD1a, and polyclonal serum anti S-100 protein. The phenotype of HX cells has been analysed using a panel of mAbs against HLA class I A, B, C monomorphic determinants, locus A and B, beta 2-microglobulin, HLA class II distinct monomorphic determinants, DP, DQ, DR, intercellular adhesion molecule-1 (ICAM-1) and vitronectin receptors. Our results indicate that HX cells express HLA class I and II, including locus A, locus B and DP, DQ, DR, like their normal counterpart (represented by Langerhans cells) and detectable levels of ICAM-1 but not vitronectin receptors. We would like to stress the possibility of the association of HX and Hodgkin's lymphoma extending the immunophenotypic profile of HX cells.
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PMID:Histiocytosis X arising in Hodgkin's disease: immunophenotypic characterization with a panel of monoclonal antibodies. 170 28

The responsiveness to IL-4 with and without costimulation with anti-IgM antibodies or phorbolester was studied in 35 cases of low grade non-Hodgkin lymphoma by analyzing enhancement of CD23 and HLA class II expression. The predominant phenotype responds directly to IL-4. Separate differentiation states can be distinguished according to coordinate or differential upregulation of CD23 and HLA class II molecules by IL-4 alone, and differences in responsiveness to anti-IgM antibodies. A particular subgroup of B-lymphoma cells defines a separate stage of B-cell differentiation. They fail to express high affinity binding sites for IL-4 and accordingly do not respond to IL-4-mediated signals. Cross-linking membrane IgM receptors or direct activation of protein kinase C via phorbolester induces IL-4 receptor expression and subsequent IL-4 reactivity.
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PMID:Regulation of IL-4 responsiveness in lymphoma B cells. 183 95

The cell line HDLM-2 was established from the pleural effusion of a patient with Hodgkin's disease. Here, we describe the morphological, cytochemical, enzymological, immunological, molecular biological, and functional characteristics of the cell line. The results of this multiparameter profile show that HDLM-2 is different from other well-studied leukemia-lymphoma cell lines including other Hodgkin's disease derived cell lines. HDLM-2 cultures contain mainly mono- or binucleated cells, but also prominent giant cells with two to ten nuclei. HDLM-2 cells do not express an immunophenotype characteristic of a given cell lineage. However, the cells are positive for Ki-1, HeFi-1, Leu-M1, Tac, and HLA class II markers. Cytochemical, enzymological, and functional data are equally inconclusive, but are definitely not compatible with a monocyte/macrophage profile. Analysis of the gene status documents that T-cell receptor beta- and gamma-chain genes are rearranged while immunoglobulin heavy chain genes are in germline configuration. The combined results indicate a T-cell origin of HDLM-2 cells. The evidence available from this and other established Hodgkin's disease derived cell lines suggests a lymphoid origin of Hodgkin and Reed-Sternberg cells.
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PMID:Characterization of Hodgkin's disease derived cell line HDLM-2. 260 52

A monoclonal antibody-secreting hybridoma cell line, VCD-1, was derived from the fusion of murine myeloma cells with splenocytes from a BALB/c mouse that had been immunised with chronic B-lymphocytic leukaemia cells. The cells came from a patient who had developed the leukaemia approximately 10 years after a course of radiotherapy for nodular sclerosing Hodgkin's disease. The antibody bound to a 30,000-dalton protein that was present in normal and malignant B cells, in monocytes, neutrophils, and interdigitating reticulum cells, and in malignant cells present in Hodgkin's disease lymph nodes. The reactive epitope was not accessible to antibody in viable intact cells; binding to peripheral blood cells could only be seen if the cells were fixed. The antibody recognises a determinant that probably resides on the alpha-chain of HLA class II molecules.
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PMID:A monoclonal antibody to an antigen present in cells from a patient with Hodgkin's disease. 331 34

The reactive cell population in Hodgkin's disease consists of predominantly CD4+ helper T cells and lacks CD8+ cytotoxic T cells and natural killer cells. This lack of a CD8+ response is surprising in view of the expression of the latent Epstein-Barr viral protein LMP by Reed-Sternberg cells in many cases of Hodgkin's disease, Deficient HLA class I expression would be one possible mechanism to avoid a CD8+ cytotoxic immune response. To test this possibility we studied the expression of HLA class I and II determinants on Reed-Sternberg cells in tissue sections and cell suspensions of Hodgkin's disease. Frozen tissue sections of 40 cases and cytocentrifuge preparations from cell suspensions of 10 lymph nodes involved by Hodgkin's disease were studied with monoclonal antibodies reactive with HLA determinants. As a control frozen tissue sections of two cases of infectious mononucleosis were studied. Careful examination of the tissue sections and subsequently of cytospins of cell suspensions showed that the Reed-Sternberg cells frequently lacked HLA class I but showed strong staining for HLA class II. Absence of HLA class I expression on Reed-Sternberg cells and their variants provides an explanation for the lack of a CD8+ cytotoxic immune response against antigens expressed on Reed-Sternberg cells.
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PMID:Absence of HLA class I expression by Reed-Sternberg cells. 751 95

Molecular typing of HLA class II loci has been performed on a sample of 196 patients with Hodgkin lymphoma. Division of patients into two histological categories--nodular sclerosing Hodgkin disease versus all other types--shows significant overall association of the nodular sclerosing group with the HLA class II region. Haplotypes and alleles defined for the four loci typed--DRB1, DQA1, DQB1, and DPB1--were present in both excess and deficit in the nodular sclerosing sample. Some of the effects are attributable to particular DRB1 and DQB1 alleles, while other effects are best explained by haplotypes marking the entire class II region. The latter effects might be due to variation in additional, as-yet-unexamined loci in the class II region or to particular combinations of alleles from two or more loci. These data also explain why earlier studies showed HLA linkage but not association, and they substantiate the specific involvement of the immune system in certain neoplastic diseases.
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PMID:Localization of predisposition to Hodgkin disease in the HLA class II region. 811 19

Hodgkin's disease is characterized by an immune response in the involved tissues that is predominantly CD4 mediated. The CD4+ T-cells are CD45RO+ and CD45RBdim, they express several activation markers but lack CD26, and in vitro can be stimulated to produce gamma-interferon and IL-4, but not IL-2. This is not the usual immunophenotype and cytokine production pattern of Th1, Th2 or Th0 cells and may be a reflection of anergy. The cause of such an anergic reaction is not clear since RS cells express HLA class II as well as the co-stimulator molecules CD80 and CD86. It is possible that a (hypothetical) super antigen expressed on the RS cells may play a role. The absence of IL-2 production however explains the absence of a CD8 mediated response. In addition to that, RS cells generally do not express HLA class I, which allows them to escape CD8 mediated responses. The link between the ineffective immune response in the tissue and the generalized immune deficiency in Hodgkin's disease may consist of several components. These include the influx of mature T-cells into the affected tissues, the secretion of inhibitory molecules by the neoplastic cells and the spill-over of the anergic T-cell response into the general circulation by either the Hodgkin related antigen or also as a result of an IL-4 dominated response. The latter possibility may also be related to the hyper-gamma-globulinaemia and the frequently observed high IgE levels.
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PMID:Immunology of Hodgkin's disease. 892 39

The HLA class II alleles were analyzed by the PCR-SSP technique in the DNA samples obtained from 27 Thai patients with non Hodgkin's lymphoma (NHL). It was found that (1) the incidence of HLA-DRB1*15 and HLA-DRB1*09 was slightly decreased (P > 0.05). On the other hand, the incidence of HLA-DQB1 alleles was the same as control. However, further study is suggested in order to conclude the close relationship between the presence of certain HLA class II alleles and susceptibility to NHL in Thai patients.
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PMID:A preliminary study of HLA class II alleles in Thai patients with non Hodgkin's lymphoma. 954 Mar 46

Recent years have witnessed the development of a variety of promising immunotherapies for treating patients with non-Hodgkin's lymphomas. Foremost among these advances is the exciting success of monoclonal antibodies directed against lymphocyte surface antigens. Rituximab is a chimeric (human-mouse) anti-CD20 antibody that induces responses in approximately half of the patients with relapsed indolent lymphomas and a third of patients with relapsed aggressive lymphomas when used as a single agent. Response rates appear even higher (up to 70%) for newly diagnosed patients treated with Rituximab monotherapy. Other promising antibodies for treatment of B cell malignancies include epratuzumab (anti-CD22), CAMPATH-1H (anti-CD52w), and Hu1D10 (anti-class II HLA). Even more exciting than antibody monotherapy is the prospect of combination antibody therapy (e.g. rituximab + epratuzumab) or combination chemotherapy and antibody therapy. In this regard, a recent phase III randomized trial from the GELA group in France demonstrated statistically significantly superior complete and overall response rates and superior event-free and overall survivals for elderly patients with newly diagnosed diffuse aggressive B cell lymphomas treated with CHOP + rituximab compared with CHOP alone. Confirmatory cooperative group trials combining chemotherapy with antibody therapies are currently underway. Another approach to augment the efficacy of antibodies is to deploy them in radiolabeled form. Iodine-131, Yttrium-90, and Copper-67 labeled monoclonal antibodies targeting CD-20, CD-22, HLA class II, and other cell surface antigens have been tested and demonstrate higher overall response rates (50-80%) and complete response rates (20-40%) than unlabeled antibodies. Pilot studies combining radiolabeled antibodies with either standard dose chemotherapy or myeloablative chemoradiotherapy with stem cell transplantation also appear very promising. Lymphoma vaccines have also produced very encouraging results in single institution studies at Stanford and the National Cancer Institute, with responding patients demonstrating superior event-free and overall survival than historical controls. Phase III randomized trials of idiotype vaccines are currently underway and novel new vaccine approaches are also being tested.
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PMID:Immunotherapy of Non-Hodgkin's lymphomas. 1172 86

The HLA region has long been implicated in sporadic and familial Hodgkin disease (HD), with recent case-control studies suggesting that HLA class II loci predispose to sporadic nodular sclerosis HD (NSHD). To determine whether this predisposition extends to familial HD, HLA class II loci (DRB1, DQA1, DQB1, DRB3, DRB4, and DRB5) and transporter associated with antigen processing (TAP) loci (TAP1, TAP2) were investigated in 100 members of 16 families with at least 2 confirmed cases of HD. With the use of the transmission disequilibrium test, evidence for linkage disequilibrium with familial HD and, in particular, familial NSHD was obtained for the DRB1*1501-DQA1*0102-DQB1*0602 haplotype, the TAP1 allele encoding Ile at residue 333, and the DRB5-0101 allele. These 3 markers were in linkage disequilibrium and may not represent independent susceptibility regions. Use of a family-based approach excludes population stratification as an explanation for these findings.
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PMID:HLA-DR, HLA-DQ, and TAP genes in familial Hodgkin disease. 1178 Dec 55


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