Impaired interleukin regulation of the phytohemagglutinin response in Hodgkin's disease

Zamkoff, Kenneth W.; Reeves, William G.; Paolozzi, Frank P.; Poiesz, Bernard J.; Comis, Robert L.; Tomar, Russell H.

doi:10.1016/0090-1229(85)90084-4

Cited by 23 publications

(5 citation statements)

References 20 publications

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“…Similar observations of low IL-2 production and/or IL-2R expression in HD blood lymphocytes have been reported by us and others (Zamkoff et al, 1985;Soullillou et al, 1985;Joshi et al, 1987). However, comparatively normal IL-2 mediated splenic lymphocyte functions, irrespective of the invasion of the tissue by malignant cells, has not been previously reported.…”

supporting

confidence: 75%

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

Mukhopadhyaya

Advani²,

Gangal³

1987

Br J Cancer

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supporting

confidence: 75%

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

Mukhopadhyaya

Advani²,

Gangal³

1987

Br J Cancer

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“…Furthermore, it is known that monocytes produce increased amounts of PGE 2 in these patients (53,54). We show that the transcriptional profile of CD4 + T cells in patients with Hodgkin's lymphoma has significant similarities to CD4 + T cells of healthy donors treated with PGE 2 .…”

Section: Pge 2 Leads To Inhibition Of Cd4mentioning

confidence: 70%

Prostaglandin E2 Impairs CD4+ T Cell Activation by Inhibition of lck: Implications in Hodgkin's Lymphoma

et al. 2006

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Many tumors, including Hodgkin's lymphoma, are associated with decreased cellular immunity and elevated levels of prostaglandin E 2 (PGE 2 ), a known inhibitor of CD4 + T cell activation, suggested to be involved in immune deviation in cancer. To address the molecular mechanisms tumor-derived PGE 2 might have on primary human CD4 + T cells, we used a whole genome-based transcriptional approach and show that PGE 2 severely limited changes of gene expression induced by signaling through the T cell receptor and CD28. This data suggests an interference of PGE 2 at an early step of T cell receptor signaling: indeed, PGE 2 stimulation of T cells leads to inactivation of lck and reduced phosphorylation of ZAP70. Antiapoptotic genes escaped PGE 2 -induced inhibition resulting in partial protection from apoptosis in response to irradiation or Fas-mediated signaling. As a functional consequence, PGE 2 -treated CD4 + T cells are arrested in the cell cycle associated with up-regulation of the cyclin/cyclin-dependent kinase inhibitor p27 kip1 . Most importantly, CD4 + T cells in Hodgkin's lymphoma show similar regulation of genes that were altered in vitro by PGE 2 in T cells from healthy individuals. These data strongly suggest that PGE 2 is an important factor leading to CD4 + T cell impairment observed in Hodgkin's lymphoma. (Cancer Res 2006; 66(2): 1114-22)

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“…However, upon addition of exogenous IL-2, lymphocytes from about half of the HD patients showed an increase in 3H-TdR incorporation but none showed an increase in T cell colony formation (Mukhopadhyaya et al, 1987b). Other investigators have also reported similar abnormalities in IL-2 mediated events in T cell activation in HD (Ford et al, 1984;Soulillou et al, 1985;Zamkoff et al, 1985).…”

mentioning

confidence: 69%

Affinity of IL-2 receptors and proliferation of mitogen activated lymphocytes in Hodgkin's disease

Damle¹,

Tatake²,

Advani³

et al. 1990

Br J Cancer

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Impaired interleukin regulation of the phytohemagglutinin response in Hodgkin's disease

Cited by 23 publications

References 20 publications

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

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

Prostaglandin E2 Impairs CD4+ T Cell Activation by Inhibition of lck: Implications in Hodgkin's Lymphoma

Affinity of IL-2 receptors and proliferation of mitogen activated lymphocytes in Hodgkin's disease

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