Melanoma cells express Fas ligand: Implications for tumor immune escape

Hahne, Meryl; Rimoldi, Donata; Schröter, Michael; Romero, Pablo Ortiz; French, Lars E.; Cerottini, J C; Tschopp, J

doi:10.1016/s0165-2478(97)86388-2

Cited by 2 publications

(2 citation statements)

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“…Fas-FasL interactions have been implicated as the mechanism behind clonal deletion after in vivo exposure to superantigen and peptide (7), controlling T cell expansion during immune responses (6), and killing by cytotoxic T cells (8). It has also been shown that FasL plays an important role in tumor biology, since a growing number of tumors have been found to express functional FasL as a protective mechanism against the Fas ϩ cells of the immune system (9,10).…”

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confidence: 99%

Antiinflammatory Effects of CD95 Ligand (FasL)-induced Apoptosis

Yuan-fu

Herndon

Zhang

et al. 1998

The Journal of Experimental Medicine

203

156

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Apoptosis is critical to homeostasis of multicellular organisms. In immune privileged sites such as the eye, CD95 ligand (FasL)-induced apoptosis controls dangerous inflammatory reactions that can cause blindness. Recently, we demonstrated that apoptotic cell death of inflammatory cells was a prerequisite for the induction of immune deviation after antigen presentation in the eye. In this report, we examine the mechanism by which this takes place. Our results show that Fas- mediated apoptosis of lymphoid cells leads to rapid production of interleukin (IL)-10 in these cells. The apoptotic cells containing IL-10 are responsible for the activation of immune deviation through interaction with antigen-presenting cells (APC). In support of this, we found that apoptotic cells from IL-10+/+ animals fed to APC in vitro promote Th2 cell differentiation, whereas apoptotic IL-10−/− cells, as well as nonapoptotic cells, favor Th1 induction. Thus, apoptotic cell death and tolerance are linked through the production of an antiinflammatory cytokine to prevent dangerous and unwanted immune responses that might compromise organ integrity.

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mentioning

confidence: 99%

Antiinflammatory Effects of CD95 Ligand (FasL)-induced Apoptosis

Yuan-fu

Herndon

Zhang

et al. 1998

The Journal of Experimental Medicine

203

156

View full text Add to dashboard Cite

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“…In recent years, it has been found that the occurrence, development, and prognosis of tumors are closely related to CD4 + CD25 + Treg cells. Treatment measures against Treg in vivo are obviously beneficial to antitumor immunity [ 27 – 30 ]. Ideal tumor therapeutic effects can be achieved by removing Treg cells in tumor patients and regulating the migration, distribution, and function of Treg.…”

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confidence: 99%

Solanine Inhibits Immune Escape Mediated by Hepatoma Treg Cells via the TGFβ/Smad Signaling Pathway

Gao

Ying

Wang

et al. 2020

BioMed Research International

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Objective. To observe the inhibitory effect of solanine on regulatory T cells (Treg) in transplanted hepatoma mice and to study the mechanism of solanine inhibiting tumor growth. Methods. The levels of Treg cells and IL-2, IL-10, and TGFβ in the blood of patients with liver cancer were detected by flow cytometry and ELISA, respectively. A mouse hepatocellular carcinoma (HCC) graft model was established and randomly divided into four groups: control group, solanine group, TGFβ inhibitor group (SB-431542), and solanine +TGFβ inhibitor combined group. Tumor volume of each group was recorded, tumor inhibition rate was calculated, and tumor metastasis was counted. The proportion of CD4+CD25+Foxp3+ Treg in transplanted tumor tissues was detected by flow cytometry. The expression levels of Foxp3 and TGFβ in transplanted tumor tissues were detected by quantitative fluorescence PCR. Results. Compared with healthy people, Treg cells and IL-2, IL-10, and TGFβ contents in peripheral blood of liver cancer patients were increased. The results of the transplanted tumor model in mice showed that the tumor volume of the transplanted mice in the solanine group and the TGFβ inhibitor mice was reduced compared with the control group. The combined group had the smallest tumor volume. The proportion of CD4+CD25+Foxp3+ Treg in the transplanted tumor tissues of mice in the solanine treatment group was significantly lower than that in the control group. The expressions of Foxp3 and TGFβ in the transplanted tumor tissues of mice in the solanine group were significantly lower than those in the control group. Conclusion. Solanine may enhance the antitumor immune response by downregulating the proportion of CD4+CD25+ Treg and the expression of Foxp3 and TGFβ in tumor tissues.

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Melanoma cells express Fas ligand: Implications for tumor immune escape

Cited by 2 publications

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Antiinflammatory Effects of CD95 Ligand (FasL)-induced Apoptosis

Antiinflammatory Effects of CD95 Ligand (FasL)-induced Apoptosis

Solanine Inhibits Immune Escape Mediated by Hepatoma Treg Cells via the TGFβ/Smad Signaling Pathway

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