01922nas a2200157   4500000000100000008004100001100001100042700001500053700001600068245011300084856007900197300000800276490000600284520146000290022001401750       2015                            d1 aBoer M1 aJoosten SA1 aOttenhoff T00aRegulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination.  uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4426762/pdf/fimmu-06-00217.pdf  a2170 v63 a<p>Regulatory T-cells (Tregs) act at the interface of host and pathogen interactions in human infectious diseases. Tregs are induced by a wide range of pathogens, but distinct effects of Tregs have been demonstrated for different pathogens and in different stages of infection. Moreover, Tregs that are induced by a specific pathogen may non-specifically suppress immunity against other microbes and parasites. Thus, Treg effects need to be assessed not only in homologous but also in heterologous infections and vaccinations. Though Tregs protect the human host against excessive inflammation, they probably also increase the risk of pathogen persistence and chronic disease, and the possibility of disease reactivation later in life. Mycobacterium leprae and Mycobacterium tuberculosis, causing leprosy and tuberculosis, respectively, are among the most ancient microbes known to mankind, and are master manipulators of the immune system toward tolerance and pathogen persistence. The majority of mycobacterial infections occur in settings co-endemic for viral, parasitic, and (other) bacterial coinfections. In this paper, we discuss recent insights in the activation and activity of Tregs in human infectious diseases, with emphasis on early, late, and non-specific effects in disease, coinfections, and vaccination. We highlight mycobacterial infections as important models of modulation of host responses and vaccine-induced immunity by Tregs.</p>
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