T and B-RFC inhibiting factor in plasma from patients with active Hodgkin's disease

Ezdinli, Ediz Z.; Simonson, Kathi L.; Simonson, Lloyd G.; Wasser, Larry P.

doi:10.1002/1097-0142(197907)44:1<106::aid-cncr2820440119>3.0.co;2-7

Cited by 10 publications

References 14 publications

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Multivariate analysis of T-cell functional defects and circulating serum factors in hodgkin's disease

Schulof

Bockman

Garofalo

et al. 1981

Cancer

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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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Multivariate analysis of T-cell functional defects and circulating serum factors in hodgkin's disease

Schulof

Bockman

Garofalo

et al. 1981

Cancer

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Rosette and blastogenesis inhibition by plasma from Hodgkin's disease and other malignancies: Positive correlation in stage I and II Hodgkin's disease

Sinclair

Ezdinli

Boonlayangoor

et al. 1983

Cancer

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The simultaneous presence of both rosette‐and mitogen‐induced blastogenesis inhibitors was measured in the plasma from 29 patients with active Hodgkin's disease, 21 patients with advanced lung cancer, nine patients with diffuse histiocytic lymphoma, 25 patients with non‐Hodgkin's lymphoma, and 17 patients with a variety of solid tumors. Only patients with active Hodgkin's disease consistently demonstrated factors which interfered with both rosetting and mitogenesis when normal allogeneic cells were utilized. While a similar proportion of patients with early and late Hodgkin's disease possessed plasma which could inhibition both tests, a significant correlation between these tests was observed only in Stage I and II disease. Varying degrees of inhibition of these tests was also observed when plasmas from patients with other malignancies were tested. Both lung cancer and histiocytic lymphoma plasma contained a factor which was capable of significantly inhibiting in the rosette assay when compared to normal human serum. Plasma from these patients also demonstrated inhibition of blastogenesis, but unlike Hodgkin's disease, no correlation between these activities could be demonstrated. Neither patients with diffuse or nodular lymphocytic lymphoma nor patients with solid tumors had significant plasma inhibition in either assay.

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Abnormal immunoregulation in remission Hodgkin disease

et al. 1985

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Peripheral blood mononuclear cells from 11 patients with remission Hodgkin disease and 20 normal controls were incubated with irradiated allogeneic lymphocytes in one-way mixed lymphocyte cultures. Simultaneously, modified assays were performed by adding supplemental irradiated PBM, T lymphocytes, or adherent cells autologous to the responders. Baseline allogeneic responsiveness of patients and controls was not different. However, significant suppression (p less than .01) was demonstrated when the cultures were supplemented with patient mononuclear cells or adherent cells, an effect not found with similar supplemental cells from controls. Conversely, T-cell supplementation of control cultures produced more than twofold increases in proliferation but significantly less augmentation in the patients' cultures (p less than .01). T-cell subset analysis in six patients showed decreased helper: suppressor cell ratios. Hodgkin disease patients have adherent suppressor cells, which persist during remission, as well as a defect in T-cell helper function.

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T and B-RFC inhibiting factor in plasma from patients with active Hodgkin's disease

Cited by 10 publications

References 14 publications

Multivariate analysis of T-cell functional defects and circulating serum factors in hodgkin's disease

Multivariate analysis of T-cell functional defects and circulating serum factors in hodgkin's disease

Rosette and blastogenesis inhibition by plasma from Hodgkin's disease and other malignancies: Positive correlation in stage I and II Hodgkin's disease

Abnormal immunoregulation in remission Hodgkin disease

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