Transforming growth factor beta 1 messenger RNA in Reed-Sternberg cells in nodular sclerosing Hodgkin's disease.

Newcom, Samuel R.; Gu, Liqun

doi:10.1136/jcp.48.2.160

Cited by 59 publications

(33 citation statements)

References 13 publications

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“…TARC (CCL17), IL-13, CD80, CD86, and CD40-CD40L interactions all contribute to the formation of tumor infiltrating T cells. HRS cells also produce some immunosuppressive factors (IL-10, TGF-b, galectin-1, and prostaglandin E2) [69][70][71], whereas CD95/FAS ligand expressed by HRS cells stimulate the apoptosis of activated Th1 and CD8 þ T cells. Tregs also produce IL-10, which indirectly contributes to the protection against cytotoxic T and NK cells [63].…”

Section: Tumor Infiltrating T Cells Hrs Cells Are Surrounded Mostly Bmentioning

confidence: 99%

Immunologic pathomechanism of Hodgkin's lymphoma

Jóna

Szodoray

Illés

2013

Experimental Hematology

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Section: Tumor Infiltrating T Cells Hrs Cells Are Surrounded Mostly Bmentioning

confidence: 99%

Immunologic pathomechanism of Hodgkin's lymphoma

Jóna

Szodoray

Illés

2013

Experimental Hematology

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“…[20][21][22] IL-9, among other cytokines, has been proposed to be involved in the fibrosis seen in NSHL. 23 When comparing subtypes, a distinction could be made between NS and the other histopathological subtypes, since the highest concentrations (up to 3350 pg/ml) of IL-9 were found in the sera from patients diagnosed as NSHL (Figure 2).…”

Section: Il-9 In Serum Samplesmentioning

confidence: 99%

Increased serum levels of interleukin-9 correlate to negative prognostic factors in Hodgkin's lymphoma

et al. 2003

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Hodgkin's lymphoma (HL) is characterised by an unbalanced cytokine secretion. Many of these cytokines have been implicated in the regulation of malignant and infiltrating cells. Interleukin-9 (IL-9) has been described to act in an autocrine fashion in HL, stimulating proliferation of the malignant cells. To investigate the potential clinical implication of this observation, a novel ELISA method was used to examine the serum levels of IL-9 in lymphoma patients. High levels of IL-9 were found in the sera from patients with HL (18/44), but not in the sera from non-Hodgkin's lymphoma patients (3/21) or healthy controls. The highest serum IL-9 levels, up to 3350 pg/ml, were observed in the nodular sclerosis subtype, and there was a correlation between IL-9 levels and the negative prognostic factors advanced stage, B-symptoms, low blood Hb and high erythrocyte sedimentation rate. Furthermore, there was no correlation between serum levels of IL-9 and IL-13, a cytokine where serum levels have been speculated to be of clinical importance. This is the first report showing that IL-9 can be measured in serum samples. A novel correlation between increased serum IL-9 levels, HL and clinical features is shown, suggesting that IL-9 is a candidate factor contributing to the development of HL.

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“…This limited efficacy may be due to the secretion by H-RS cells of immunosuppressive cytokines such as transforming growth factor b (TGFb), the Th2 cytokine IL13 and the Th2 attracting chemokine TARC by HD tumors. [15][16][17] We reasoned that local delivery of IL12 to Hodgkin tumors by EBV-specific CTL could improve the antitumor activity of the infused CTL in at least three separate ways. First, CTL could deliver the potent antitumor activity of IL12 to tumor sites, without inducing the systemic toxicity associated with this cytokine.…”

mentioning

confidence: 99%

A strategy for treatment of Epstein–Barr virus-positive Hodgkin's disease by targeting interleukin 12 to the tumor environment using tumor antigen-specific T cells

et al. 2003

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Adoptive immunotherapy with Epstein-Barr virus (EBV)-specific cytotoxic T cells (CTL) is effective for the prophylaxis and treatment of EBV-induced lymphoma in hematopoietic stem cell recipients. However, in EBV-positive Hodgkin's disease (HD) the efficacy of adoptively transferred EBV-specific CTL may be limited by tumor-derived immunosuppressive factors, such as T-cell growth factor (TGF) b, interleukin (IL)13 and the chemokine TARC. Local delivery of IL12 to tumor sites by tumor-specific CTL could provide direct antitumor effects and overcome the CTL-inhibitory effects of the Th2 tumor environment while avoiding the systemic toxicity of recombinant IL12. EBV-specific CTL transduced with a retrovirus vector expressing the p40 and p35 subunits of IL12 as a single molecule (Flexi-IL12), produced IL12 following antigenic stimulation. This resulted in an elevated production of Th1 cytokines, including interferon g and tumor necrosis factor a, and a reduction in the Th2 cytokines IL4 and IL5. Flexi-IL12-transduced CTL resisted the antiproliferative and anticytotoxic effects of exogenous TGFb, likely by antagonizing the TGFb-induced downregulation of the Th1 transcriptional factor T-bet. In addition, Flexi-IL12-transduced CTL demonstrated a proliferative advantage in the presence of inhibitory supernatants from HD-derived cell lines. Tumor-specific, Flexi-IL12-transduced EBV-specific CTL should have a functional advantage over unmodified CTL, particularly in the presence of the adverse Th2 cytokine environment produced by Hodgkin tumor cells.

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Transforming growth factor beta 1 messenger RNA in Reed-Sternberg cells in nodular sclerosing Hodgkin's disease.

Abstract: Aims-To determine the cellular origin of the most potent cytokine present in Hodgkin's disease, transforming growth factor (TGF)

Cited by 59 publications

References 13 publications

Immunologic pathomechanism of Hodgkin's lymphoma

Immunologic pathomechanism of Hodgkin's lymphoma

Increased serum levels of interleukin-9 correlate to negative prognostic factors in Hodgkin's lymphoma

A strategy for treatment of Epstein–Barr virus-positive Hodgkin's disease by targeting interleukin 12 to the tumor environment using tumor antigen-specific T cells

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