Expression of interferon‐gamma receptors and interferon‐gamma‐induced up‐regulation of intercellular adhesion molecule‐1 in basal cell carcinoma; decreased expression of IFN‐γR and shedding of ICAM‐1 as a means to escape immune surveillance

Kooy, Angela J. W.; Tank, Bhupendra; Vuzevski, V. D.; Joost, Theodoor van; Prens, Errol P.

doi:10.1002/(sici)1096-9896(199802)184:2<169::aid-path976>3.3.co;2-7

Cited by 10 publications

(15 citation statements)

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“…19 Soluble ICAM-1 level is higher in patients with liver metastasis than in patients without liver metastasis. 34 Both tumor-and host-derived sICAM-1 promote immune escape 35 and angiogenic activity, 36 supporting tumor growth. Expression of LFA-1 is a heterogeneous property of C26 cells that endows cancer cells with increased angiogenesis-stimulating potential.…”

Section: Discussionmentioning

confidence: 99%

Colon Carcinoma Cell Interaction With Liver Sinusoidal Endothelium Inhibits Organ-Specific Antitumor Immunity Through Interleukin-1-Induced Mannose Receptor in Mice

et al. 2010

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Mannose receptor (ManR)-mediated liver sinusoidal endothelial cell (LSEC) endocytosis plays a role in antigen presentation and innate immunity, but its role in hepatic metastasis is unknown. We studied ManR-mediated endocytosis during C26 colorectal cancer cell interaction with LSECs and its implications in metastasis. Uptake of labeled ManR ligands (mannan and ovalbumin) and immunohistochemistry were used to study ManR endocytosis and expression. Several interleukin (IL)-1 inhibitors and the cyclooxygenase-2 (COX-2) inhibitor celecoxib were used to analyze the role of IL-1 and COX-2 in ManR regulation. Anti-mouse ManR antibodies and ManR knockout (ManR 2/2 ) mice were used to identify ManR-dependent mechanisms during antitumor immune response of liver sinusoidal lymphocytes (LSLs) interacting with tumor-activated LSECs. ManR expression and endocytosis increased in tumor-activated LSECs through a two-step mechanism:(1) Release of COX-2-dependent IL-1-stimulating factors by lymphocyte function-associated antigen-1-expressing C26 cells in response to intercellular adhesion molecule-1 (ICAM-1), which was expressed and secreted by tumor-activated LSECs; and (2) widespread up-regulation of ManR in LSECs through tumor-induced IL-1. In addition, LSLs that had interacted with tumoractivated LSECs in vivo decreased their antitumor cytotoxicity and interferon (IFN)-gamma secretion while they increased IL-10 release ex vivo. IFN-gamma/IL-10 ratio also decreased in the hepatic blood from tumor-injected mice. Immunosuppressant effects of tumor-activated LSECs on LSLs were abrogated in both LSECs from ManR 2/2 mice and tumor-activated LSECs given antimouse ManR antibodies. Conclusion: ICAM-1-induced tumor COX-2 decreased antitumor activity during hepatic metastasis through IL-1-induced ManR. ManR constituted a common mediator for prometastatic effects of IL-1, COX-2, and ICAM-1. A rise in hepatic IFN-gamma/IL-10 ratio and antitumor cytotoxicity by way of ManR blockade is consistent with the antimetastatic effects of IL-1, COX-2, and ICAM-1 inhibitors. These data support ManR and ManR-stimulating factors as targets for hepatic colorectal metastasis therapy. (HEPATOLOGY 2010;51:2172-2182 Abbreviations: ASMA, alpha-smooth muscle actin; CM, cell-conditioned medium; COX-2, cyclooxygenase-2; CSPG, chondroitin sulfate proteoglycan; ELISA, enzyme-linked immunosorbent assay; FITC-OVA, fluorescein isothiocyanate-labeled ovalbumin; FSA, formaldehyde treated serum albumin; ICAM-1, intercellular adhesion molecule-1; ICE, IL-1-converting enzyme; IgG2a, immunoglobulin G2a; IL, interleukin; IL-1RI, IL-1 receptor type I; IL-1Ra, IL-1 receptor antagonist; LFA-1, lymphocyte function-associated antigen 1; LSEC, liver sinusoidal endothelial cell; LSL, liver sinusoidal lymphocyte; ManR, mannose receptor; ManR À/À , ManR knockout; SD, standard deviation; sICAM-1, soluble ICAM-1.From the

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Section: Discussionmentioning

confidence: 99%

Colon Carcinoma Cell Interaction With Liver Sinusoidal Endothelium Inhibits Organ-Specific Antitumor Immunity Through Interleukin-1-Induced Mannose Receptor in Mice

et al. 2010

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“…hepatocellular carcinoma, prostatic carcinoma, basal cell carcinoma) do not express both receptor chains, thus providing tumour resistance to IFNg (Kooy et al, 1998;Nagao et al, 2000;Royuela et al, 2000), we proved whether the TGCT unresponsiveness to endogenous IFNg is due to the absence of IFNgR. Applying nonradioactive ISH and immunohistochemistry, however, IFNgR mRNA and protein for both a and b chains were detected in primary TGCT.…”

Section: Discussionmentioning

confidence: 99%

Malignant germ cell tumours of the testis express interferon-γ, but are resistant to endogenous interferon-γ

et al. 2003

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Cytokines possess discrepant effects on tumour cells varying from anti-to proapoptotic activities. We recently reported that testicular germ cell tumours (TGCT) express a functional form of the proinflammatory cytokine interferon-gamma (IFNg). The present study asked whether TGCT-derived IFNg influences survival or death of neoplastic germ cells. Analysis of TGCT cell lines demonstrated that they expressed and secreted IFNg, but were resistant to the endogenous IFNg since neutralisation of IFNg by a specific blocking antibody had no influence on the proliferation and/or the degree of apoptosis of tumour cells. To study mechanisms providing tumour resistance to endogenous IFNg, we analysed primary TGCT and two human TGCT cell lines (NTERA and NCCIT) for the expression of IFNg receptor and for the level of phosphorylation of the signal transducer and activator of transcription (STAT)-1. In situ hybridisation, immunocytochemistry, Western blot analysis and flow cytometry indicated that primary TGCT as well as NCCIT and NTERA cell lines expressed the heterodimeric cell surface IFNg receptor which consists of both 90-kDa a-and the 85-kDa b-chains. However, the downstream transcription factor STAT-1 was not phosphorylated constitutively, indicating that STAT-1 is not activated by the endogenous IFNg. Upon application of recombinant human IFNg in excess, however, STAT-1 was phosphorylated and the interferon regulatory factor-1 (IRF-1) was induced, suggesting that both IFNgR and STAT-1 are functionally intact in TGCT. Altogether our results suggest that despite secreting biologically active IFNg, the concentration of the endogenous IFNg is too low to stimulate the IFNgR/STAT signalling pathway in TGCT in an autocrine and/or paracrine manner.

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“…Previous studies have established that testicular germ cell tumour cells can express both mRNA and protein of IFN-g and the expressed IFN-g is able to induce the chemokine IP-10, indicating its biological activity, whereas it is not able to phosphorylate the downstream STAT1 (Schweyer et al, 2002(Schweyer et al, , 2003. A number of tumours and tumour cell lines have also been reported to develop a permanent and selective IFN-g insensitivity, such as testicular germ cell tumours, RCC cell line, basal cell carcinoma of the skin and human lung adenocarcinoma cell lines (Kooy et al, 1998;Dovhey et al, 2000;Nagao et al, 2000;Schweyer et al, 2002Schweyer et al, , 2003Dunn et al, 2005b). Such insensitivity to IFN-g is due to lack of expression of IFN-g receptors or the receptor downstream genes.…”

Section: Western Blot Analysismentioning

confidence: 99%

Expression of interferon-γ in human adrenal gland and kidney tumours

Zhang

Nie

et al. 2007

Br J Cancer

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It is known that interferon-g (IFN-g) is produced by activated T and NK lymphoid cells, mononuclear cells, and macrophage and dendritic cells. Our previous studies have shown that IFN-g-like immunoreactivity also appears in human adrenal cortical tumour and phaeochromocytoma. To investigate whether human tumour cells can produce IFN-g, we examined 429 biopsy specimens of 30 kinds of tumour and tumour-surrounding tissues in adrenal glands and in kidneys by using immunohistochemistry and in situ hybridisation. IFN-g immunoactivity was shown in 34.3% of the adrenal cortical adenomas, 50% of the adrenal cortical carcinomas, 26.7% of the phaeochromocytomas, 26.7% of the clear cell renal cell carcinomas (RCCs), 22% of the adrenal cortexes and 40% of medullas adjacent to tumours. The positive samples and expression areas were well overlapped between the IFN-g mRNA and the immunohistochemistry staining. Western blot analysis has further confirmed the immunohistochemistry results by showing a distinct IFN-g band corresponding to 17.4 kDa in tissue extracts from adrenal cortical adenoma, phaeochromocytoma and clear cell RCCs. These results indicate that IFN-g is produced by some types of tumour cells, suggesting it may play a dual role in the development of these tumours.

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Expression of interferon‐gamma receptors and interferon‐gamma‐induced up‐regulation of intercellular adhesion molecule‐1 in basal cell carcinoma; decreased expression of IFN‐γR and shedding of ICAM‐1 as a means to escape immune surveillance

Cited by 10 publications

References 0 publications

Colon Carcinoma Cell Interaction With Liver Sinusoidal Endothelium Inhibits Organ-Specific Antitumor Immunity Through Interleukin-1-Induced Mannose Receptor in Mice

Colon Carcinoma Cell Interaction With Liver Sinusoidal Endothelium Inhibits Organ-Specific Antitumor Immunity Through Interleukin-1-Induced Mannose Receptor in Mice

Malignant germ cell tumours of the testis express interferon-γ, but are resistant to endogenous interferon-γ

Expression of interferon-γ in human adrenal gland and kidney tumours

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