Autologous Mixed Lymphocyte Reaction in Patients with Hodgkin's Disease

Eg, Engleman; Cj, Benike; Rt, Hoppe; Hs, Kaplan; Fr, Berberich

doi:10.1172/jci109828

Cited by 121 publications

(49 citation statements)

References 45 publications

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“…Increased spontaneous suppression of proliferative responses has been found in HD (Twomey et al, 1975;Goodwin et al, 1977;Twomey et al, 1980;Hillinger & Hertzig, 1978;Engleman, 1979) and may contribute to the defect in cell mediated immunity which is characteristic of patients with this disease. Con A-induced suppression of lymphocyte proliferation is either normal (Van Haelen & Fisher, 1981) or decreased (Schulof et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

“…In HD there is an increase in suppressor activity for proliferation induced by mitogens (Goodwin et al, 1977;Twomey et al, 1980;Schulof et al, 1981) or cell bound alloantigens (Twomey et al, 1975;Hillinger & Hertzig, 1978;Engleman et al, 1979) which may contribute to the defect in cell-mediated immunity present in these patients (Twomey et al, 1975;Schulof et al, 1981). All these studies, however, have employed peripheral blood mononuclear cells (PB-MNC) and little information is available on the regulatory activity of tissue lymphocytes in this disease.…”

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confidence: 99%

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Spontaneous and Concanavalin A-induced suppressor activity in control and Hodgkin's disease patients

Akbar¹,

Jones²,

Wright³

1984

Br J Cancer

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Indirect evidence suggests that abnormal regulation of B cells exists in Hodgkin's disease (HD) due, perhaps, to the sequestration of regulatory T-lymphocyte subpopulations in the spleen in this condition. Other work implicates the B-cell itself in this abnormality. In this study we have attempted to measure regulatory T-cell function by quantitating spontaneous and Concanavalin A(Con A)-induced suppressor activity in T-enriched spleen cells from control and HD spleens for pokeweed mitogen(PWM)-induced immunoglobulin (Ig) production. Using this polyclonal system, HD patients' spleen T-lymphocytes could not be shown to differ markedly from the control series. Cells capable of spontaneous and mitogen-induced modulation of Ig synthesis were present in both populations and showed a reciprocal relationship implying the activation of the same cell type. In this respect HD and control spleen resembled peripheral blood. A limited parallel investigation of PWM-regulatory activity in cells from spleen and peripheral blood from individual patients was also undertaken. Individual patients showed wide variation in suppression between the two compartments and, therefore, measurements of functional capacity in blood alone may not provide a true estimate of total regulatory capacity in lymphoma patients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Spontaneous and Concanavalin A-induced suppressor activity in control and Hodgkin's disease patients

Akbar¹,

Jones²,

Wright³

1984

Br J Cancer

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“…The AMLR has been found to be deficient or absent in patients with various immunologic disorders such as systemic lupus erythematosus (14)(15)(16)(17), primary biliary cirrhosis (1 8), Sjogren's syndrome (1 91, several cancers (20), chronic lymphocytic leukemia (1,21), infectious mononucleosis (22), Hodgkin's disease (23), and Kaposi's sarcoma (24). The suppressive effect of aging on the AMLR has also been reported (25)(26)(27).…”

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confidence: 99%

Impaired killer cell generation in the autologous mixed leukocyte reaction by rheumatoid arthritis lymphocytes

Goto

Zvaifler

1985

Arthritis & Rheumatism

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Natural killer‐like cells are generated along with interleukin‐2 (IL‐2) in the autologous mixed leukocyte reaction (AMLR). Patients with active rheumatoid arthritis (RA), but not those whose disease is in remission, are poor producers of AMLR killer cells. This defect cannot be explained by age, medications, or serum factors. The impaired generation of natural killer‐like cells was not influenced by γ‐interferon but could be partially restored by addition of indomethacin to the AMLR culture, or by culturing RA T cells with exogenous IL‐2. However, the response of RA T cells to IL‐2 was significantly less than that of controls. These results suggest that the defect in the generation of AMLR killer cells in patients with active RA may be due in part to defective production of IL‐2 and a lesser sensitivity of RA T cells to IL‐2.

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“…To understand M+ functions during the immune response, these subpopulations need to be characterized and their functional relationships established. Subpopulation delineation is critical in studies involving tumor-bearing hosts (TBH), because tumor growth changes the immunoregulatory properties of M+ (6)(7)(8)(9)(10)(11)(15)(16)(17)(18)24,25,28,33,35,36) and changes also occur in M+ phenotype and function. Phenotypic changes in TBH M+ include changes in surface antigen (Mac-1, Mac-2, Mac-3, and Ia) expression (9)(10)(11)16,19,25,34), size distribution (341, and peroxidase staining (11).…”

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confidence: 99%

“…Phenotypic changes in TBH M+ include changes in surface antigen (Mac-1, Mac-2, Mac-3, and Ia) expression (9)(10)(11)16,19,25,34), size distribution (341, and peroxidase staining (11). Concomitant functional changes in TBH M+ include decreased accessory cell function in the allogeneic mixed lymphocyte reaction (MLR) (6,10,11,16,24), the autologous mixed lymphocyte reaction (AMLR) (8,35,36), and mitogen-induced T cell proliferation (7,9,10,25,33). These functional changes result from an altered suppressor M+ population (9,11,16,25,(34)(35)(36) and a decreased production of enhancing factors (18,28,35).…”

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confidence: 99%

Two‐color flow cytometric analysis of the expression of MAC and MHC Class II antigens on macrophages during tumor growth

1990

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Tumor-bearing host (TBH) macrophages (M+) exhibit immune dysfunction that is concomitant with phenotypic changes. We examined M+ subpopulations by changes in the expression of surface antigens Mac-1, -2, -3, and Ia on normal and TBH peritoneal and splenic M+. M+ were double-labeled and analyzed by flow cytometry to observe multiple expression of surface antigens. Tumor growth alters the multiple expression of these M+ markers. Peritoneal and splenic M+ had different Mac+ and Mac+Ia+ population percentages. In TBH, peritoneal M+ had decreased percentages of Mac-1+2+, Mac-1+3+, Mac-2+3+, and Mac+Ia+ M+. This decrease correlated with functional changes in TBH M+. In contrast, there was an increase in Mac-2-Ia-TBH peritoneal M+. Previously undiscovered Mac-1+2-3-and Mac-1-2-3+ populations were found. In contrast to peritoneal M+, there was an increase in the percentage of Mac-l+2+, Mac-1+3+, and Mac-2+3+ splenic TBH M+ but, like peritoneal M+, there was a decrease in the percentage of Mac+Ia+ M+. Also, TBH splenic M+ showed a smaller but more uniform antigen density than normal host splenic M+. Tumor growth modulated phenotypic alterations in peritoneal and splenic M+ subpopulations. Combined with earlier functional studies of M 4 subpopulations, these data suggested a relationship between changes in M+ phenotype and tumor-induced dysfunction of M+-modulated immune activity.Key terms: Macrophage surface antigens, double-label techniques, monoclonal antibodies, Mac-1, Mac-2, Mac-3, Ia, tumor-bearing host Macrophages (M+) have diverse functions that may reflect the existence of distinct subpopulations of M+ (9-11,16,29-31,341. To understand M+ functions during the immune response, these subpopulations need to be characterized and their functional relationships established. Subpopulation delineation is critical in studies involving tumor-bearing hosts (TBH), because tumor growth changes the immunoregulatory properties of M+ (6)(7)(8)(9)(10)(11)(15)(16)(17)(18)24,25,28,33,35,36) and changes also occur in M+ phenotype and function. Phenotypic changes in TBH M+ include changes in surface antigen (Mac-1, Mac-2, Mac-3, and Ia) expression (9)(10)(11)16,19,25,34), size distribution (341, and peroxidase staining (11). Concomitant functional changes in TBH M+ include decreased accessory cell function in the allogeneic mixed lymphocyte reaction (MLR) (6,10,11,16,24), the autologous mixed lymphocyte reaction (AMLR) (8,35,36), and mitogen-induced T cell proliferation (7,9,10,25,33). These functional changes result from an altered suppressor M+ population (9,11,16,25,(34)(35)(36) and a decreased production of enhancing factors (18,28,35). If the phenotype of the suppressor M+ could be identified (reported here) and then correlated with its specific function, a greater understanding of the mechanism of TBH M+-mediated control of immune reactivity would emerge.

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Autologous Mixed Lymphocyte Reaction in Patients with Hodgkin's Disease

Cited by 121 publications

References 45 publications

Spontaneous and Concanavalin A-induced suppressor activity in control and Hodgkin's disease patients

Spontaneous and Concanavalin A-induced suppressor activity in control and Hodgkin's disease patients

Impaired killer cell generation in the autologous mixed leukocyte reaction by rheumatoid arthritis lymphocytes

Two‐color flow cytometric analysis of the expression of MAC and MHC Class II antigens on macrophages during tumor growth

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