5 research outputs found
Cross-border trafficking in human beings: prevention and intervention strategies for reducing sexual exploitation
Over the years, growing attention has been given to the phenomenon of trafficking in human beings (THB). Sexual exploitation was until recently by far the most commonly identified feature of THB, followed by forced labour. Many activities to combat trafficking for the purpose of sexual exploitation have been initiated by numerous supranational, international as well as national organizations. Much is written about these initiatives, but some areas have been neglected. Knowledge on âwhat worksâ is in particular limited. The growing attention to THB entails a demand for more information. The severity of the crime and the impact on its victims makes it of utmost importance to gain more insight into the working and effectiveness of anti-trafficking strategies and interventions. The main objective of this review was to assess the presently available evidence on the effects of interventions that aim to prevent and suppress trafficking in human beings
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The Anti-inflammatory Protein TSG-6 Regulates Chemokine Function by Inhibiting Chemokine/Glycosaminoglycan Interactions.
TNF-stimulated gene-6 (TSG-6) is a multifunctional protein secreted in response to pro-inflammatory stimuli by a wide range of cells, including neutrophils, monocytes, and endothelial cells. It has been shown to mediate anti-inflammatory and protective effects when administered in disease models, in part, by reducing neutrophil infiltration. Human TSG-6 inhibits neutrophil migration by binding CXCL8 through its Link module (Link_TSG6) and interfering with the presentation of CXCL8 on cell-surface glycosaminoglycans (GAGs), an interaction that is vital for the function of many chemokines. TSG-6 was also found to interact with chemokines CXCL11 and CCL5, suggesting the possibility that it may function as a broad specificity chemokine-binding protein, functionally similar to those encoded by viruses. This study was therefore undertaken to explore the ability of TSG-6 to regulate the function of other chemokines. Herein, we demonstrate that Link_TSG6 binds chemokines from both the CXC and CC families, including CXCL4, CXCL12, CCL2, CCL5, CCL7, CCL19, CCL21, and CCL27. We also show that the Link_TSG6-binding sites on chemokines overlap with chemokine GAG-binding sites, and that the affinities of Link_TSG6 for these chemokines (KD values 1-85 nm) broadly correlate with chemokine-GAG affinities. Link_TSG6 also inhibits chemokine presentation on endothelial cells not only through a direct interaction with chemokines but also by binding and therefore masking the availability of GAGs. Along with previous work, these findings suggest that TSG-6 functions as a pluripotent regulator of chemokines by modulating chemokine/GAG interactions, which may be a major mechanism by which TSG-6 produces its anti-inflammatory effects in vivo