Functional evaluation of T-lymphocytes from peripheral blood and spleens in Hodgkin's disease

Mukhopadhyaya, Robin; Advani, SH; Gangal, S. G.

doi:10.1038/bjc.1987.293

Cited by 11 publications

(5 citation statements)

References 12 publications

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“…HHV‐6 exists in two variants, A and B, the latter being more prevalent, and is activated under various immunocompromised conditions 1–5. Suppression of cell‐mediated immunity in both Hodgkin's disease (HD) and non‐Hodgkin's lymphoma (NHL) is well documented 6,7. In this study, activation of HHV‐6 in 98 untreated patients diagnosed at presentation with either HD ( n = 39) or NHL ( n = 59) was studied by polymerase chain reaction (PCR) detection of viral DNA in plasma fractions.…”

Section: Introductionmentioning

confidence: 99%

Activation of HHV‐6 in Lymphoproliferative Disorders: A Polymerase Chain Reaction‐Based Study

Tailor

Saikia

Advani

et al. 2004

Annals of the New York Academy of Sciences

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HHV-6 is a latent herpes virus persisting throughout the adult life of the infected host in an integrated form and is often activated in immunocompromised situations. Detection of HHV-6 DNA in the plasma of an individual indicates the presence of active viral replication in the host. Because lymphomas are known to be associated frequently with host immunosupression, we studied activation of HHV-6 in 98 patients diagnosed with Hodgkin's disease (HD) or non-Hodgkin's lymphoma (NHL). HHV-6 activation was documented in 34% of cases of non-Hodgkin's lymphoma and 39% of those of Hodgkin's disease; however, no correlation of activation status with pathological types of Hodgkin's disease and between copy numbers in peripheral blood mononuclear cell DNA and the corresponding plasma DNA was noticeable.

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Section: Introductionmentioning

confidence: 99%

Activation of HHV‐6 in Lymphoproliferative Disorders: A Polymerase Chain Reaction‐Based Study

Tailor

Saikia

Advani

et al. 2004

Annals of the New York Academy of Sciences

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“…The possible mechanisms of impairment of CMI associated with active HD include an intrinsic defect of T cells, serum inhibitory factors and activation of suppressor monocytes or lymphocytes. We have investigated most of these aspects of T cell deficiencies and their regulation (Gulwani et al, 1986;Karande et al, 1982;Moghe et al, 1980Moghe et al, , 1981Mukhopadhyaya et al, 1983Mukhopadhyaya et al, , 1987a and also the Interleukin-2 (IL-2) mediated events in HD (Damle et al, 1990;Gangal et al, 1987;Joshi et al, 1987;Mukhopadhyaya et al, 1987b).…”

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confidence: 99%

Natural killer and lymphokine activated killer cell functions in Hodgkin's disease

Rajaram¹,

Tatake²,

Advani³

et al. 1990

Br J Cancer

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Summary We report the natural killer (NK) and lymphokine activated killer (LAK) cell activities in peripheral blood lymphocytes (PBL) from untreated patients with Hodgkin's disease (HD) and from healthy donors. The frequency of LAK cell precursors was also studied using limiting dilution analysis (LDA). About 75% of the HD patients had normal NK activity. There was a higher percentage of low NK responders (mean percent NK activity of healthy donors -2 SD) in patients with lymphocyte depletion histologic grade of the disease and those who were in clinical stage IV, suggesting a correlation of decrease in NK activity with poor prognosis. We found efficient LAK activity against the NK-sensitive K562 cells and NK-resistant VIP (melanoma) and T-24 (bladder carcinoma) tumour targets in both low and normal NK responder HD patients, irrespective of the histopathological grade and clinical stage of the disease. In concordance with their good LAK cell activity, HD patients showed a frequency distribution of LAK cell progenitors in the PBL comparable to that of healthy donors.

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“…WANEBO et al (3) and by us (19,20,32). Disparity between the immunoreactivity of cells from different lymphoid compartments has also been shown before (7,24,32).…”

Section: Discussionmentioning

confidence: 56%

“…Disparity between the two post activation events such as proliferative response and production of 11^2 by lymphoid cells in cancer patients has been shown earlier by HARGErr et al (6). WANEBO et al (3) and by us (19,20,32). Disparity between the immunoreactivity of cells from different lymphoid compartments has also been shown before (7,24,32).…”

Section: Discussionmentioning

confidence: 59%

lnterleukin‐2 mediated regulation of mitogen‐activated T cell reactivity from different lymphoid sources in patients with squamous cell carcinoma of the oral cavity

Murali¹,

Somasundaram²,

Rao

et al. 1989

J Oral Pathology Medicine

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Peripheral blood lymphocytes (PBL) from patients with oral cancer (treated and untreated), oral leukoplakia and healthy donors; lymphocytes from metastatic and non-metastatic lymph nodes (met LNL and non-met LNL); and tumor infiltrating lymphocytes (TIL) were tested for proliferative response to mitogen PHA (phytohemagglutinin) and its augmentation by recombinant Interleukin-2 (rIL-2), for expression of Tac antigen (CD25) and for production of IL-2. Depressed PHA responses were found in PBL of treated and untreated patients, and in TIL. Addition of IL-2 could bring about 16% to 31% augmentation in lymphocyte response to PHA from all the three sources. PBL from 50% of healthy donors, 45% of patients with leukoplakia, 25% untreated oral cancer patients and 35% treated oral cancer patients showed IL-2 mediated augmentation of PHA response. While, 40% non-met LNL samples, 70% met LNL samples and only 23% TIL samples showed increased mitogen induced proliferation by IL-2. The augmented levels of PHA response of PBL from treated and untreated patients, and of TIL, were still below those of normal PBL. PBL from patients with leukoplakia, treated oral cancer patients and TIL showed depressed CD25 antigen expression. Depressed IL-2 production was observed only in PBL of leukoplakia patients. Thus the IL-2 mediated events of T cell activation from different lymphoid sources in patients with oral cancer did not correlate with their proliferative responses.

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Functional evaluation of T-lymphocytes from peripheral blood and spleens in Hodgkin's disease

Cited by 11 publications

References 12 publications

Activation of HHV‐6 in Lymphoproliferative Disorders: A Polymerase Chain Reaction‐Based Study

Activation of HHV‐6 in Lymphoproliferative Disorders: A Polymerase Chain Reaction‐Based Study

Natural killer and lymphokine activated killer cell functions in Hodgkin's disease

lnterleukin‐2 mediated regulation of mitogen‐activated T cell reactivity from different lymphoid sources in patients with squamous cell carcinoma of the oral cavity

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