TRANSLATION IN LIBEL CASES: REPUTATIONS AT STAKE!

Abstract: In this paper we examine translation arising in court cases involving reputational damage. A diachronic and tightly focused cross-jurisdictional selection of examples from case law is used to highlight the range of ways in which translation can be employed, blamed, or relied upon by the parties and by the courts, and we glimpse how translations can be a source of libel, a defence against libel, or a gateway to libellous material, how crucial translation can be in protecting or damaging reputations, and how significantly it can affect a case’s outcome. We apply Engberg’s lens for communication in legal contexts, distinguishing micro, meso and macro occurrences of translation at publisher/business/individual, judicial, and State levels. Recurring translation-related topics either mooted by courts or arising in our analysis are then outlined, including: competing translations; translation techniques; translator identification; online translation; how the acceptance of jurisdiction may be influenced by translation requirements; and how judges approach decision-making when foreign language documents and translation are involved.Abstract: In this paper we examine translation arising in court cases involving reputational damage. A diachronic and tightly focused cross-jurisdictional selection of examples from case law is used to highlight the range of ways in which translation can be employed, blamed, or relied upon by the parties and by the courts, and we glimpse how translations can be a source of libel, a defence against libel, or a gateway to libellous material, how crucial translation can be in protecting or damaging reputations, and how significantly it can affect a case’s outcome. We apply Engberg’s lens for communication in legal contexts, distinguishing micro, meso and macro occurrences of translation at publisher/business/individual, judicial, and State levels. Recurring translation-related topics either mooted by courts or arising in our analysis are then outlined, including: competing translations; translation techniques; translator identification; online translation; how the acceptance of jurisdiction may be influenced by translation requirements; and how judges approach decision-making when foreign language documents and translation are involved

Characterization of human IL-35+ regulatory T cells induced by Rhinovirus-treated dendritic cells

IL-35 ist ein Heterodimer, bestehend aus EBV-induziertem Gen 3 (EBI3) und p35, einer der beiden Untereinheiten von IL-12. Dieses Zytokin wurde kürzlich als inhibitorisch beschrieben und wird von den natürlich regulatorischen T-Zellen der Maus, jedoch nicht von denen des Menschen produziert. In dieser Dissertation wird gezeigt, dass Dendritische Zellen, die mit humanem Rhinovirus (HRV) aktiviert sind (R-DZs), die Produktion und Freisetzung von IL-35 in humanen T-Zellen induzieren. Werden T-Zellen mit R-DZs kokultiviert, wird in den T-Zellen eine supprimierende Funktion auf andere T-Zellen beobachtet. Sowohl in CD4+ als auch in CD8+ T-Zellen des peripheren Blutes, jedoch nicht in aus humanem Nabelschnurblut gewonnenen naiven T-Zellen, konnte diese inhibierende Funktion durch R-DZs induziert werden. Weiters wird gezeigt, dass der Zellkulturüberstand von T-Zellen des peripheren Blutes (CD4+ als auch CD8+ T-Zellen), die mit R-DZs kokultiviert wurden, inhibierend ist. Diese Beobachtung lässt den Schluss zu, dass die Effekte nicht durch Zell-Zell-Kontakt, sondern durch lösliche Faktoren hervorgerufen wurden. Die klassischen immun-inhibitorischen Zytokine IL-10, TGF-ß oder IFN-α waren jedoch nicht für diesen Effekt verantwortlich, da ein Blockieren dieser Faktoren durch Antikörper nichts an der hemmenden Eigenschaft des Zellkulturüberstandes änderte. Wir konnten mittels qPCR, Durchflusszytometrie und Immun-Präzipitation zeigen, dass IL-35 von mit R-DZs kokultivierten T-Zellen produziert und freigesetzt wird. Ein Blockieren der beiden IL-35 Untereinheiten (EBI3 und p35) mit Antikörpern gegen diese Strukturen konnte die Hemmung aufheben. Damit wird gezeigt, dass IL-35 für die inhibitorische Eigenschaft des Zellkulturüberstandes verantwortlich ist. Depletion von IL-35 aus dem zuvor hemmenden Zellkulturüberstand führte ebenso zum Verlust dieser Funktion. Die Induktion dieser IL-35 produzierenden T-Zellen (IL-35+ T-Zellen) durch R-DZs zeigte keine Korrelation mit erhöhter Foxp3 Expression. Dies könnte ein Hinweis darauf sein, dass keine klassischen regulatorischen T-Zellen induziert werden. Durch das Hochregulieren der inhibitorischen Oberflächenmoleküle B7-H1 (CD274) und Sialoadhesin (CD169) sind R-DZs schlechte T-Zell-Stimulatoren. Als wir diese beiden Oberflächenmoleküle mit Antikörpern, die gegen diese Strukturen gerichtet sind, blockierten, verhinderten wir die Induktion von IL-35. Wir schließen daraus, dass ein kombinatorisches Signal der R-DZs, vermittelt durch B7-H1 und Sialoadhesin, an die T-Zellen für die Induktion der IL-35+ T-Zellen verantwortlich ist. Unsere Ergebnisse beschreiben einen neuen Weg und seine Bausteine in der Induktion von immun-inhibitorischen T-Zellen. IL-35 wird zum ersten Mal als inhibitorisches Zytokin im Humansystem nachgewiesen. Weiters bekommen wir Einblick in die Strategien von HRV, dem Haupterreger des Schnupfens, dem Immunsystem zu entgehen.IL-35 is a heterodimer of EBV-induced gene 3 (EBI3) and of the p35 subunit of IL-12, which has recently been identified as an inhibitory cytokine produced by natural regulatory T cells in mice, but not in humans. Here we demonstrate that dendritic cells (DCs) activated by human rhinoviruses (R-DCs) induce IL-35 production and release in human T cells. The first finding of this thesis was that R-DCs induce a suppressor function in cocultured T cells. This suppressor function was induced in CD4+ and CD8+ T cells derived from human peripheral blood but not in naïve T cells from cord blood. It was further observed that the cell culture supernatant (SN) of peripheral blood T cells (both CD4+ and CD8+) cocultured with R-DCs had an inhibitory effect on T cells. Therefore the inhibition was not cell-cell contact dependent and we focused on soluble factors. When we blocked the classical inhibitory cytokines including IL-10, TGF-ß or IFN-α with antibodies against the respective factors, the SN was still inhibitory. Therefore the inhibition was not caused by the release of these cytokines. Via qPCR, flow cytometry and immuno-precipitation it was shown that, R-DC-induced regulatory T cells produced and released IL-35. When we blocked the inhibitory SN with Abs against either subunit of IL-35, the inhibitory effect was gone. Hence IL-35 was responsible for the inhibitory effect of the SN. In addition, the p35 depleted SN was no longer inhibitory. The induction of IL-35 producing T cells (IL-35+ regulatory T cells) by R-DCs did not correlate with an increased Foxp3 expression, indicating that R-DCs do not induce classical regulatory T cells. In order to determine which structures on R-DCs influence the generation of IL-35+ regulatory T cells, blocking antibodies against R-DCs inhibitory surface molecules B7-H1 (CD274) and sialoadhesin (CD169) were added. Most importantly we observed that, when we blocked B7-H1 and sialoadhesin on the R-DC side with specific mAb against both receptors, the induction of IL-35 was prevented. Thus, the combinatorial signal delivered by R-DCs to T cells via B7-H1 and sialoadhesin is crucial for the induction of human IL-35+ regulatory T cells, defining a new route of T-cell instruction. These results demonstrate a novel pathway and its components for the induction of immune-inhibitory T cells and show for the first time that IL-35 is immune-inhibitory in humans. The findings of this thesis contribute to a better understanding of immune evasion strategies of human rhinoviruses (HRV) the major cause of the common cold

IMMUNOLOGY IN CROATIA 40th anniversary of the Croatian Immunological Society

This special issue is dedicated to the 40th Anniversary of organized activities of the Croatian Immunological Society. On this occasion the Annual Meeting of Croatian Immunological Society will be organized in [ibenik, October 9-12 2008, where this supplement will be introduced and distributed. The idea for such a collection of data was born (conceived) during my first presidency 10 years ago, when the first account of Croatian Immunological Society activities was published, in Croatian. This time, we have tried to include not only the founding and activities of Croatian Immunological Society but also all research groups working in the field of immunology in Croatia during the past 40 years. I wish to express my warmest thanks to all authors for their contributions. Especially for collecting all the relevant data, references and achievements of their research groups. From the collected data it is evident that Immunology in Croatia developed very fast (rapidly), and achieved a prominent place among scientific disciplines. Both national and international collaboration resulted in the establishment of new groups, not only at universities where immunology first started, but also at several institutes and hospitals in Zagreb and Rijeka. The number of Croatian Immunological Society members varies, being always more than one hundred and less than two hundred, but with a very good renewal rate of young members each year. We hope that, with improved financing policy of basic science in Croatia, more novices will be attracted, and that immunologists will remain as active as they were throughout this past 40 years, despite some quite untoward conditions. Sabina Rabatić guest edito

CLARIN. The infrastructure for language resources

CLARIN, the "Common Language Resources and Technology Infrastructure", has established itself as a major player in the field of research infrastructures for the humanities. This volume provides a comprehensive overview of the organization, its members, its goals and its functioning, as well as of the tools and resources hosted by the infrastructure. The many contributors representing various fields, from computer science to law to psychology, analyse a wide range of topics, such as the technology behind the CLARIN infrastructure, the use of CLARIN resources in diverse research projects, the achievements of selected national CLARIN consortia, and the challenges that CLARIN has faced and will face in the future. The book will be published in 2022, 10 years after the establishment of CLARIN as a European Research Infrastructure Consortium by the European Commission (Decision 2012/136/EU)

CLARIN

The book provides a comprehensive overview of the Common Language Resources and Technology Infrastructure – CLARIN – for the humanities. It covers a broad range of CLARIN language resources and services, its underlying technological infrastructure, the achievements of national consortia, and challenges that CLARIN will tackle in the future. The book is published 10 years after establishing CLARIN as an Europ. Research Infrastructure Consortium

CLARIN

The book provides a comprehensive overview of the Common Language Resources and Technology Infrastructure – CLARIN – for the humanities. It covers a broad range of CLARIN language resources and services, its underlying technological infrastructure, the achievements of national consortia, and challenges that CLARIN will tackle in the future. The book is published 10 years after establishing CLARIN as an Europ. Research Infrastructure Consortium