Now showing 1 - 10 of 11
  • 2000Journal Article
    [["dc.bibliographiccitation.firstpage","384"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","390"],["dc.bibliographiccitation.volume","292"],["dc.contributor.author","Fayyazi, Afshin"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Eichmeyer, B."],["dc.contributor.author","Herms, J."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Berger, H."],["dc.date.accessioned","2018-11-07T10:34:41Z"],["dc.date.available","2018-11-07T10:34:41Z"],["dc.date.issued","2000"],["dc.description.abstract","Granuloma annulare, a prototype noninfectious granulomatous dermatitis, is morphologically characterized by a necrobiotic core surrounded by a cellular infiltrate, Because of many morphological similarities to tuberculosis, granuloma annulare has been suggested to represent a delayed-type hypersensitivity (Th1) reaction in the course of which inflammatory cells elicit matrix degradation, In the present study we (1) investigated the expression of interferon-gamma as the most important Th1-associated cytokine, (2) sought in situ evidence for the coexpression of the proinflammatory cytokine tumor necrosis factor-a and cytokine-regulated matrix metalloproteinases 2 (gelatinase A) and 9 (gelatinase B), and (3) sought to determine whether shrunken cells seen within necrobiotic areas of granuloma annulare are apoptotic cells, In situ hybridization combined with immunofluorescence showed that large numbers of infiltrating CD3(+) lymphocytes express interferon-gamma, Application of catalyzed signal amplification in immunodetection revealed that the vast majority of CD3(+) lymphocytes and CD68(+) macrophages contained tumor necrosis factor-alpha. Immunohistochemistry demonstrated that macrophages producing tumor necrosis factor-ct coexpress matrix metalloproteinases 2 and 9, In situ end-labeling combined with immunofluorescence detected few apoptotic T cells in perivascular regions and numerous apoptotic macrophages within necrobiotic areas, These results suggest that in granuloma annulare interferon-gamma(+) Th-1 lymphocytes may cause a delayed-type hypersensitivity reaction whereby macrophages are differentiated to aggressive effector cells expressing tumor necrosis factor-alpha and matrix metalloproteinases, In parallel, activation-induced apoptosis in lymphocytes and macrophages may serve to restrict the destructive potential of the inflammatory cells."],["dc.identifier.doi","10.1007/s004030000150"],["dc.identifier.isi","000088939700003"],["dc.identifier.pmid","10994772"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44932"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.title","Expression of IFN gamma, coexpression of TNF alpha and matrix metalloproteinases and apoptosis of T lymphocytes and macrophages in granuloma annulare"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2007Journal Article
    [["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","81"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Bachem, A."],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Steinfelder, Hans Juergen"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Wagner, W."],["dc.contributor.author","Pottek, T."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hopker, W. W."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:59:10Z"],["dc.date.available","2018-11-07T10:59:10Z"],["dc.date.issued","2007"],["dc.description.abstract","Testicular germ cell tumours (TGCT) represent the most common malignancy in young males. We reported previously that two prototype members of the mitogen-activated protein kinase (MAPK) family, the MAPK ERK kinase (MEK) and extracellular signal-regulated kinase (ERK), are inactive in malignant testicular germ cells and become active after drug stimulation, leading to apoptosis of tumour cells. In this study, we asked whether the protein phosphatase PP2A, a known inhibitor of the MEK-ERK pathway, participates in the proliferation and/or apoptosis of primary TGCT (n = 48) as well as two TGCT cell lines (NTERA and NCCIT). Quantitative RT-PCR, immunohistochemistry, western blot analyses and phosphatase assay indicate that primary TGCT as well as TGCT cell lines express PP2A and that PP2A is active in TGCT cell lines. The inhibition of PP2A by application of two PP2A inhibitors, cantharidic acid (CA) and okadaic acid (OA), results in a significant increase in caspase-3-mediated apoptosis of TGCT cell lines. Thereby, PP2A inhibition was accompanied by phosphorylation and activation of MEK and ERK. Functional assays using the MEK inhibitor PD98059 demonstrated that the phosphorylation of NIEK and ERK was required for the induction of caspase-3-mediated apoptosis of malignant germ cells. Thus, our data suggest that inhibition of PP2A mediates its apoptosis-inducing effect on TGCT through activation of the MEK-ERK signalling pathway that leads to caspase-3-mediated apoptosis of tumour cells. In addition our results support previous observations that PP2A exerts an anti-apoptotic effect on malignant tumour cells. Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.2203"],["dc.identifier.isi","000249181800009"],["dc.identifier.pmid","17590861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50636"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Expression and function of protein phosphatase PP2A in malignant testicular germ cell tumours"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2007Conference Abstract
    [["dc.bibliographiccitation.firstpage","317"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pathology - Research and Practice"],["dc.bibliographiccitation.lastpage","318"],["dc.bibliographiccitation.volume","203"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Jaenisch, S."],["dc.contributor.author","Baumhoer, D."],["dc.contributor.author","Fayyazi, Afshin"],["dc.contributor.author","Radzun, H.-J."],["dc.date.accessioned","2018-11-07T11:07:22Z"],["dc.date.available","2018-11-07T11:07:22Z"],["dc.date.issued","2007"],["dc.identifier.isi","000247312300164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52540"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.issn","0344-0338"],["dc.title","Expression of CXCR3 in malignant testicular germ cell tumours"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2004Journal Article
    [["dc.bibliographiccitation.firstpage","589"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Meschter, O."],["dc.contributor.author","Heintze, A."],["dc.contributor.author","Zschunke, F."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schlott, T."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:46:28Z"],["dc.date.available","2018-11-07T10:46:28Z"],["dc.date.issued","2004"],["dc.description.abstract","Testicular germ cell tumours (TGCT) represent the most common malignancies in young males. Whereas in 1970s, the survival rate in patients with metastatic testicular tumours was only 5%, these days, 80% of the patients treated by modern chemotherapy will survive their disease. The drug that revolutionised the cure rate for patients with metastatic testicular tumours was cisdiamminedichloroplatinum ( cisplatin, CDDP). In vitro experiments on neoplastic germ cell lines showed that their exquisite sensitivity to CDDP could be attributed to p53-dependent and -independent pathways. Applying cDNA macroarray, semiquantitative RT-PCR and Western blot analyses, blocking experiments, caspase activity assays, and morphological methods, we sought here to define the p53-independent pathway(s) involved in the CDDP-induced apoptosis. For this purpose, we used the human TGCT cell line NCCIT, the mutated p53 of which is known to remain inactive during the course of CDDP-induced apoptosis. Our experiments showed that within hours of CDDP application, two prototype members of the 'mitogen-activated protein kinase' ( MAPK) family, designated 'MAPK ERK kinase' (MEK) and 'extracellular signal-regulated kinase' ( ERK), were dually phosphorylated and caspase-3 became active. Functional assays using MEK inhibitors demonstrated that the phosphorylation of MEK and ERK was required for the activation of caspase-3 as the executing caspase. Interestingly, experiments with the human malignant germ cell line NTERA, which is known to possess wild-type p53, revealed the same results. Thus, our data suggest that CDDP mediates its p53-independent apoptosis-inducing effect on the malignant human testicular germ cells - at least partially - through activation of the MEK - ERK signalling pathway."],["dc.identifier.doi","10.1038/sj.bjc.6601919"],["dc.identifier.isi","000222930400029"],["dc.identifier.pmid","15266324"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47752"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0007-0920"],["dc.title","Cisplatin-induced apoptosis in human malignant testicular germ cell lines depends on MEK/ERK activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2003Journal Article
    [["dc.bibliographiccitation.firstpage","915"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","921"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Peters, J."],["dc.contributor.author","Wagner, A."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:36:22Z"],["dc.date.available","2018-11-07T10:36:22Z"],["dc.date.issued","2003"],["dc.description.abstract","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 (IFNgamma). The present study asked whether TGCT-derived IFNgamma influences survival or death of neoplastic germ cells. Analysis of TGCT cell lines demonstrated that they expressed and secreted IFNgamma, but were resistant to the endogenous IFNgamma since neutralisation of IFNgamma 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 IFNgamma, we analysed primary TGCT and two human TGCT cell lines (NTERA and NCCIT) for the expression of IFNgamma 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 alpha- and the 85-kDa beta-chains. However, the downstream transcription factor STAT-1 was not phosphorylated constitutively, indicating that STAT-1 is not activated by the endogenous IFNgamma. Upon application of recombinant human IFNgamma in excess, however, STAT-1 was phosphorylated and the interferon regulatory factor-1 (IRF-1) was induced, suggesting that both IFNgammaR and STAT-1 are functionally intact in TGCT. Altogether our results suggest that despite secreting biologically active IFNgamma, the concentration of the endogenous IFNgamma is too low to stimulate the IFNgammaR/STAT signalling pathway in TGCT in an autocrine and/or paracrine manner."],["dc.identifier.doi","10.1038/sj.bjc.6601209"],["dc.identifier.isi","000185074900023"],["dc.identifier.pmid","12942126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45305"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0007-0920"],["dc.title","Malignant germ cell tumours of the testis express interferon-gamma, but are resistant to endogenous interferon-gamma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article
    [["dc.bibliographiccitation.firstpage","222"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Immunology"],["dc.bibliographiccitation.lastpage","230"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:32:12Z"],["dc.date.available","2018-11-07T10:32:12Z"],["dc.date.issued","2002"],["dc.description.abstract","The morbidity and lethality of tuberculosis is partially the result of an ineffective delayed-type hypersensitivity reaction which causes caseating granulomas in the lung and other organs. Recently we showed that during caseation besides macrophages numerous Fas(+) FasL(+) lymphocytes undergo apoptosis and postulated that this phenomenon may be due to activation-induced cell death (AICD) as a consequence of T-lymphocyte reactivation via bacillary antigens. As purified protein derivative of Mycobacterium tuberculosis (Mtb-PPD) provokes caseation in tuberculosis patients, the question arose as to whether bacillary antigens are responsible for AICD within caseous areas. In the present study Mtb-PPD-specific T helper 1 (Th1)-differentiated T lymphocytes were generated in vitro, Reactivation of these cells with Mtb-PPD resulted in a concentration-dependent hyporesponsiveness, which was due to an increase in apoptosis of gammadelta(+), alphabeta(+) CD4(+) as well as alphabeta(+) CD8(+) T lymphocytes as assessed by the demonstration of the apoptosis-associated mitochondrial membrane protein 7A6 and DNA fragmentation. Blocking experiments demonstrated that Mtb-PPD antigens exploited the Fas/FasL system to induce apoptosis in Mtb-PPD-specific T lymphocytes. These results may support the hypothesis that in tubercle granulomas with caseation T lymphocytes undergo AICD following reactivation by bacillary antigens, thus contributing to the persistence of tuberculosis."],["dc.identifier.doi","10.1046/j.0019-2805.2001.01355.x"],["dc.identifier.isi","000173866100013"],["dc.identifier.pmid","11872098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44290"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0019-2805"],["dc.title","Mycobacterial antigens induce apoptosis in human purified protein derivative-specific up T lymphocytes in a concentration-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2000Journal Article
    [["dc.bibliographiccitation.firstpage","255"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","259"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Mihm, Sabine"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Hartmann, Hans"],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:25:22Z"],["dc.date.available","2018-11-07T10:25:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Background-Pathogenesis of hepatitis C virus (HCV) associated Liver injury is thought to be due to the host antiviral immune response. Using a quantitative, competitive RT-PCR technique, we recently showed that expression of interferon gamma (IFN-gamma) and IFN-gamma inducible type of nitric oxide synthase (iNOS) is increased in homogenised liver tissue of patients with chronic HCV infection. Aims--To determine the cellular origin of IFN-gamma and iNOS expression and to examine the hypothesis that T cell derived IFN-gamma secretion induces iNOS in hepatocytes in chronic HCV infection. Methods--By applying a non-radioactive in situ hybridisation method combined with indirect immunofluorescence, 33 liver biopsy specimens from patients with chronic HCV infection were studied for cellular expression of IFN-gamma and iNOS mRNA. Results--In chronic HCV infection, both IFN-gamma and iNOS gene expression were significantly increased. IFN-gamma and iNOS mRNA were observed in CD3+ lymphocytes infiltrating portal tracts and hepatic lobules, but not in hepatocytes. Conclusions-Results are consistent with previous reports that IFN-gamma and iNOS transcripts are elevated in chronic HCV infection. In contrast to the hypothesis, IFN-gamma expressing T cells do not induce iNOS in hepatocytes, but probably in T cells. T lymphocytes expressing IFN-gamma and/or iNOS have the potential to participate in autocrine and paracrine pathways that may contribute to the pathobiology of chronic hepatitis C."],["dc.identifier.doi","10.1136/gut.46.2.255"],["dc.identifier.isi","000084976700023"],["dc.identifier.pmid","10644322"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42847"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","British Med Journal Publ Group"],["dc.relation.issn","0017-5749"],["dc.title","Liver infiltrating T lymphocytes express interferon gamma and inducible nitric oxide synthase in chronic hepatitis C virus infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2000Journal Article
    [["dc.bibliographiccitation.firstpage","534"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY"],["dc.bibliographiccitation.lastpage","539"],["dc.bibliographiccitation.volume","437"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T08:58:08Z"],["dc.date.available","2018-11-07T08:58:08Z"],["dc.date.issued","2000"],["dc.description.abstract","Gout tophi are characterised by foreign body granulomas consisting of mono- and multinucleated macrophages surrounding deposits of monosodium urate microcrystals. After primary formation, granulomas grow associated with degradation of the extracellular matrix. Based on this background, we have sought (1) to investigate whether during granuloma's growth new macrophages are recruited into the tophi, (2) to find in situ evidence for macrophages' active role in matrix degradation and (3) to examine whether shrunk cells seen within gout tophi are apoptotic. Immunohistochemistry showed that perivascular localised mononuclear cells are CD68+, S100A8+, S100A9+, 25F9-, representing freshly migrated monocytes/macrophages. In contrast, almost all CD68+ mono- multinucleated cells arranged within granulomas were S100A8-, S100A9-, 25F9+, representing mature (non-migrating) macrophages. Serial sections revealed that macrophages co-express tumour necrosis factor (TNF)-alpha and matrix metalloproteinases (MMPs) 2 and 9. In situ end-labelling of fragmented DNA demonstrated that CD68+ macrophages undergo apoptosis within gout tophi. Our data show that macrophages are continuously recruited into the gout tophi. These macrophages co-produce the proinflammatory cytokine TNF-alpha and two TNF-alpha inducible lytic enzymes, MMP-2 and MMP-9, suggesting that TNF-alpha may induce MMP production followed by matrix degradation within foreign body granulomas. In parallel, macrophages undergo apoptosis, a phenomenon that may restrict the destructive potential of inflammatory macrophages."],["dc.identifier.doi","10.1007/s004280000282"],["dc.identifier.isi","000165789400009"],["dc.identifier.pmid","11147175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23573"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0945-6317"],["dc.title","Continuous recruitment, co-expression of tumour necrosis factor-alpha and matrix metalloproteinases, and apoptosis of macrophages in gout tophi"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article
    [["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","197"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Baumhoer, D."],["dc.contributor.author","Peters, J."],["dc.contributor.author","Cattaruzza, Marco"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Fayyazi, Afshin"],["dc.date.accessioned","2018-11-07T10:30:20Z"],["dc.date.available","2018-11-07T10:30:20Z"],["dc.date.issued","2002"],["dc.description.abstract","Tumour-infiltrating T lymphocytes (TILs) possess discrepant properties ranging from anti- to pro-tumour activities. Understanding precisely which mechanisms navigating T lymphocytes into the tumour site will help to further the anti-tumour or to disrupt the pro-tumour activities of TILs. The present study asked what enables TILs to migrate into testicular germ cell tumours (TGCTs). TILs were characterized and the expression of a large panel of T-lymphocyte-attracting chemokines was investigated in 21 TGCT cases. Flow cytometry revealed that approximate to 80% of TGCT-infiltrating T lymphocytes express CXCR3, a receptor for the chemokine interferon-inducible protein-10 (IP-10). RT-PCR and immunohistochemistry indicated that IP-10 was the only chemokine investigated which was constantly expressed in TGCT. As EP-10 was found to be expressed by endothelial cells of TGCT-associated blood vessels, the question arose whether the IP-10-regulating cytokine interferon-gamma (IFNgamma) is produced by tumour cells and if so, whether tumour-derived IFNgamma can induce IP-10 in endothelial cells. Applying in sitit hybridization, IFNgamma transcripts were found in neoplastic germ cells. Analyses of two TGCT cell lines indicated that the tumour cells not only express IFNgamma mRNA, but also produce and secrete IFNgamma protein; tumour-derived IFNgamma provokes IP-10 expression and secretion by endothelial cells in vitro, as assessed by PCR and ELISA. Together, the data suggest that neoplastic germ cells secret IFNgamma and thereby stimulate tumour-associated endothelial cells to express IP-10, which contributes to the recruitment of CXCR3 + T lymphocytes to the site of TGCTs. Copyright (C) 2002 John Wiley Sons, Ltd."],["dc.identifier.doi","10.1002/path.1094"],["dc.identifier.isi","000175202800013"],["dc.identifier.pmid","12081209"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43843"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Expression of CXC chemokine IP-10 in testicular germ cell tumours"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2000Journal Article
    [["dc.bibliographiccitation.firstpage","417"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","425"],["dc.bibliographiccitation.volume","191"],["dc.contributor.author","Fayyazi, Afshin"],["dc.contributor.author","Eichmeyer, B."],["dc.contributor.author","Soruri, Afsaneh"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Schwarz, P."],["dc.contributor.author","Radzun, H.-J."],["dc.date.accessioned","2018-11-07T10:37:42Z"],["dc.date.available","2018-11-07T10:37:42Z"],["dc.date.issued","2000"],["dc.description.abstract","Immunity against mycobacteria is almost exclusively confined to epithelioid cell granulomas, where a long-lasting but labile balance exists between host and bacilli. The relationship between immunity and mycobacteria results in regression, growth, or caseation of granulomas. To prove whether caseation is associated with apoptosis, biopsy specimens of patients with tuberculosis were analysed by electron microscopy and by in situ end-labelling combined with immunofluorescence. Apoptotic cells were not detected in regressive granulomas. Whereas productive granulomas without histologically recognizable caseous necrosis revealed only single apoptotic cells, large numbers of apoptotic CD68+ macrophages and apoptotic CD3+, CD45RO+ T cells were observed within caseous foci. As prime candidates undergoing and/or eliciting apoptosis, vital cells surrounding caseous foci were characterized. Immunohistochemistry showed that the majority of vital CD68+ macrophages surrounding caseous foci are negative for the anti-apoptotic protein bcl2, but positive for the pro-apoptotic protein bax. In situ hybridization combined with immunofluorescence demonstrated that the majority of the adjacent lymphocytes are activated CD3+, CD45RO+ cells expressing the pro-inflammatory cytokine interferon gamma (IFN gamma) and the death ligand FasL. These results suggest that caseation is strongly associated with apoptosis of macrophages and T lymphocytes; that the onset of apoptosis in macrophages may be promoted by the lack of bcl2 and the abundance of bax; and that activation-induced cell death (AICD) may be responsible for the apoptosis of T cells. Copyright (C) 2000 John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/1096-9896(2000)9999:9999<::AID-PATH664>3.0.CO;2-R"],["dc.identifier.isi","000088493400011"],["dc.identifier.pmid","10918217"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45632"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Apoptosis of macrophages and T cells in tuberculosis associated caseous necrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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