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)

In the autologous mixed lymphocyte reaction (AMLR), T lymphocytes are stimulated to proliferate by autologous non-T mononuclear cells. In five untreated patients with Hodgkin disease, the AMLR was diminished. In addition, in the same five patients, T cell response PHA was inhibited by a cell in the non-T cell fraction, the response of non-T cells to PWM was diminished, and there was a diminished ability of the non-T cell population to stimulate in allogeneic MLR. However, the response of T cells from patients with Hodgkin disease to allogeneic antigen was normal. The AMLR and allogeneic MLR were then studied in an additional five untreated patients before and after monocyte depletion of the stimulating non-T mononuclear cell population. In this second group of Hodgkin disease patients, the AMLR was again diminished when T cells were incubated either with non-T cells or non-T cells depleted of monocytes. In the Hodgkin patients, monocyte depletion did not alter the T cell response in the AMLR. In the controls, monocyte depletion greatly diminished the proliferative response. The diminished AMLR in untreated Hodgkin disease patients may be the result of a failure of adequate monocyte stimulation of autologous T cells.
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PMID:Diminished autologous mixed lymphocyte reaction in patients with Hodgkin disease: evidence for non-T cell dysfunction. 621 84

A factor inhibitory to PHA-induced lymphocyte blastogenesis was found to be present in the serum of a patient with advanced Hodgkin's disease and nephrotic syndrome. The inhibitory activity for both syngeneic and allogeneic lymphocytes was dependent on the presence of peripheral blood monocytes. The Raji-cell serum assay, as well as immunofluorescence and light and electron microscopy of the renal biopsy, showed no evidence of immune complexes. Nevertheless, a high serum IgE level as well as the finding that ultracentrifugation and heating at 56 degrees C significantly reduced the inhibitory activity (P less than 0.01) suggested the possibility that an immune complex might have mediated the suppressive activity. Treatment of the Hodgkin's disease with combined chemotherapy caused a marked reduction in the monocyte-dependent serum inhibitory activity which in turn coincided with a prompt remission of the nephrotic syndrome and marked regression of disease.
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PMID:Monocyte-dependent serum suppression of lymphocyte blastogenesis in Hodgkin's disease: an association with nephrotic syndrome. 621 62

Suppressor cells can be identified in vitro either by specific antibodies or by functional test assays. On investigation of the latter, a close relationship was demonstrated between spontaneously active and in vitro induced (ConA) suppressor cells. The activity of these cells, however, showed a wide day to day variation. Hence, no clinically relevant conclusions could be drawn from a comparison of patients and controls. This was shown both for SLE and myeloma. However, in multiple myeloma indirect evidence of increased activity of short-lived suppressor cells emerged from a different methodological approach. Helper and suppressor cells were evaluated using monoclonal antibodies. Patients with Hodgkin's disease in long-term remission had decreased proportions of T-lymphocytes. Helper T-cells but not suppressor T-cells were strongly diminished. The helper-suppressor ratio was changed from 2.1 in controls to 1.2 in patients. The stimulation (PHA-stimulation) index of the patients was half of the control value. The interactions of suppressor and tumour cells were investigated in non-Hodgkin's lymphoma. In general, a marked reactive infiltration of neoplastic lymph nodes was found. The pattern of suppressor cell distribution argued in favour of a functional role of these cells in tumour growth.
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PMID:[Immunologic detection and in vitro activity of suppressor cells]. 622 47

PHA-induced T lymphocyte colonies from peripheral blood mononuclear cells of untreated Hodgkin's disease (HD) patients and normal healthy donors were assayed by one-step stimulation in microagar capillary cultures. A significant depression in the T cell colony formation was observed in HD patients in comparison with normal healthy donors. Clinical staging of the disease had no influence on this abnormality. Preincubation of HD lymphocytes for 24 h in tissue culture medium did not produce any appreciable recovery in the colony formation potential. However, in the presence of 24-hour culture supernatants of HD mononuclear cells, there was significant inhibition in the colony formation by lymphocytes obtained from normal healthy donors. Significance of these observations is discussed.
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PMID:Impairment of T lymphocyte colony formation in Hodgkin's disease: effect of soluble inhibitory factors on normal T lymphocyte colony formation potential. 641 59

The present study was undertaken to elucidate the type and the role of suppressor cells on T lymphocyte response to PHA in untreated and treated patients with Hodgkin's disease. The mean value of peripheral blood T lymphocyte response to PHA in untreated or treated patients was lower than that in healthy subjects. However, the difference was not statistically significant. There was no significant difference in T lymphocyte response between localized and generalized stage or between different cell types in both active and remission Hodgkin's disease patients. The mean T lymphocyte response to PHA of active patients without systemic symptoms (A), on the other hand, was significantly higher than that of active patients with systemic symptoms (B). The mean value of T lymphocyte response in the presence of monocyte-enriched E- cells was significantly lower, whereas the mean value in the presence of monocyte-depleted E- cells was only moderately lower than that in the absence of these non-T cells in active patients. The mean value of PHA response of T lymphocytes with monocyte-enriched or monocyte-depleted E- cells was only slightly lower than PHA response without these cells in remission patients. No suppressor cell activity of T cells was observed in both active and remission patients. The only significant difference in the suppressor cell activity of monocyte-enriched E- cells on the T lymphocyte response to PHA was observed between localized and generalized stage in patients with active disease. Unlike peripheral blood monocyte-enriched E- cells, the splenic monocyte-enriched E- cells possessed no significant suppressor cell activity on the splenic T lymphocyte response to PHA in active Hodgkin's disease patients. These observations suggest that the depression of in vitro cell-mediated immunity seen in patients with active Hodgkin's disease may be due to the non-specific suppression of T lymphocyte response by monocytes, in addition to a possibly intrinsic defect of T lymphocytes.
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PMID:Role of suppressor cells in depression of T lymphocyte proliferative response in untreated and treated Hodgkin's disease. 644 26

Lymphocyte response to PHA was depressed in 9 of 14 cases of Hodgkin's disease (HD) and in 4 of 14 cases of lung carcinoma (LC). This depression was caused in one-third of the HD cases and in one-half of the LC cases by an excess of prostaglandin synthesis.
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PMID:Suppressor cells in Hodgkin's disease and lung carcinoma. 645 11

A comprehensive immunologic and serologic analysis was performed on 31 untreated patients with Hodgkin's disease. Immune evaluations stressed T-cell functional activity and included traditional parameters (PHA responsiveness and delayed hypersensitivity skin reactivity), as well as newer functional assays (T-cell colony formation, chemotaxis, spontaneous and antibody-dependent cytotoxicity, and concanavalin A-induced suppressor cell activity (CISA). Serum factors included ferritin, prostaglandins, zinc, copper, immune complexes, and thymic hormone activity. Every patient exhibited at least one T-cell or serum abnormality. The greatest percentage of patients exhibited T-cell defects in chemotaxis (85%), colony formation (81%). and PHA reactivity (64%). Immune defects were more common with advanced disease but were not related to absolute T-cell or monocyte count, skin test anergy, or abnormalities of T mu/T gamma cell proportions. Linear relationships were identified among abnormalities in the three assays employing mononuclear cells (PHA, colony formation, CISA) which may have reflected the inhibitory influence of monocytes present in the mononuclear cell preparations. Low serum zinc correlated with marked impairment of T-cell chemotaxis. Elevated prostaglandins were associated with high PHA reactivity and with depressed colony formation. Our results indicate that many complex factors, including intrinsic T-cell defects, contribute to the impaired immunity associated with Hodgkin's disease.
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PMID:Multivariate analysis of T-cell functional defects and circulating serum factors in Hodgkin's disease. 645 60

The secretion of PGE2 from monocytes of newly diagnosed patients with Hodgkin's disease (HD) was compared to that of patients in remission, who were not receiving either chemotherapy or radiotherapy, and normal controls. We found that monocyte monolayers of some patients, both newly diagnosed and those in remission, secreted markedly elevated levels of PGE2. The lymphocyte proliferative response to PHA was increased to a similar extent in both newly diagnosed patients and those in remission when cultured in the presence of indomethacin. PGE2 concentrations in the medium of mononuclear cultures correlated with the lymphocyte proliferative response to PHA (P less than 0.05). However, no correlation of monocyte PGE2 production with decreased E rosette forming lymphocytes, anergy or clinical stage could be demonstrated. We suggest that PGE2 secretion by monocytes is indicative of an 'activated' state of these cells. It is, however, unlikely that PGE2 is the only molecular species responsible for the decreased cellular immune function in HD. 'Activated' monocytes may be part of the immune response in this disease and may be responsible for the decreased cellular immunity.
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PMID:Monocyte PGE2 secretion in Hodgkin's disease and its relation to decreased cellular immunity. 657 80

In a retrospective study of non-Hodgkin's lymphomas, the 14q+ marker was found in at least one of the samples examined from 17 patients with B-cell lymphoproliferative diseases (LPD). In the PHA-stimulated cultures, the marker was found in each sample in 10%-100% of the cells. An indirect stimulation, as indicated by a 3H-thymidine incorporation and IG secretion, of normal B cells by a T-cell mitogen, such as PHA, has been recently documented. This phenomenon is confirmed by our chromosome analysis, which demonstrated characteristic chromosome changes in PHA-stimulated cultures of patients with B-cell malignancies and indicated that the phenomenon can be observed not only in normal B cells but also in malignant B cells.
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PMID:Indirect stimulation of B-cell proliferation in vitro by T cells, as evidenced by cytogenetic analysis of PHA-stimulated cell cultures of B-cell lymphomas. 660 3

Complement-fixing and non-complement-fixing circulating immune complexes were determined in 42 previously untreated Hodgkin's disease patients by Pl.A.T., C1qB-ELISA and KgB tests. The functional status of the monocyte-macrophage system was evaluated by measuring the serum lysozyme levels. These parameters were then correlated with the patient's immunocompetence, as assessed by the percentage of E-rosette forming cells and the PHA response. The Pl.A.T. was positive in 35.7% patients, the KgB-test in 34.3% and the C1qB-ELISA in 19%. There was overlapping of positive results in 37.5% patients. No correlation was found between CIC levels and stage, unfavourable histology or B symptoms. The PHA response was significantly depressed in CIC + patients, as detected by the C1qB-ELISA technique (p less than 0.0025). The data on serum lysozyme offer an insight into the possible mechanism regulating serum levels of CICs in Hodgkin's disease. Two distinct situations seem to exist: in the first, high CIC levels are associated with normal or low serum lysozyme values (p versus normal controls: n.s.); in the second, serum lysozyme levels are high and CIC absent (p less than 0.005 versus control values). The lowest lysozyme levels are also associated with a depressed lymphocyte PHA response. It could, therefore, be concluded that, in Hodgkin's disease, the presence, or absence, of CICs is directly correlated to the degree of monocyte-macrophage clearance activity and that the host's immunocompetence plays an important role in the induction and/or maintenance of this functional defect.
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PMID:Circulating immune complexes and serum lysozyme levels in untreated Hodgkin's disease. Their relationship to immune function. 664 93


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