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This article discusses the role of regulatory T-cells (Tregs) in infectious pancreatic necrosis, a complication of acute pancreatitis. The study found that Treg activation disrupts the barrier function of the duodenum, allowing bacteria to enter the pancreatic necrosis. The researchers focused on the expression of the co-inhibitory molecule Programmed-death 1 (PD-1) on Tregs and found that PD-1 expression correlated with the level of Tregs. They also conducted experiments on mouse models and found that blocking PD-1 reduced the translocation of bacteria into the pancreas. The study suggests that PD-1 blockage could be a potential therapeutic strategy for infectious pancreatic necrosis, but further research is needed. [Extracted from the article]

Background: A cluster of eleven patients, including eight family members and three healthcare workers with fever and thrombocytopenia occurred in Yixing County, Jiangsu Province, China, from October to November 1996. However, the initial investigation failed to identify its etiology. Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by SFTS bunyavirus (SFTSV), which was first discovered in 2009. The discovery of novel SFTSV resulted in our consideration to test SFTSV on the remaining samples of this cluster in September 2010. Methodology/Principal findings: We retrospectively analyzed the epidemiological and clinical data of this cluster. The first case, one 55-year-old man with fulminant hemorrhagic diseases, died on October 14, 1996. His younger brother (the second case) developed similar hemorrhagic diseases after nursing him and then died on November 3. From November 4 to November 15, nine other patients, including six family members and three medical staffs, developed fever and thrombocytopenia after exposure to the second case. The sera of six patients were collected on November 24, 1996. IgM antibodies against SFTSV were detected in all of the six patients’ sera using enzyme-linked immunosorbent assay (ELISA), while IgG antibodies were detected in one patient’s serum using an indirect immunofluorescence assay (IFA). We also found that IgG antibodies against SFTSV were still detected in four surviving patients’ sera 14 years after illness onset. Conclusions and significance: The mysterious pathogen of the cluster in 1996 was proved to be SFTSV on the basis of its epidemiological data, clinical data and serological results. It suggests that SFTSV has been circulating in China for more than 10 years before being identified in 2009, and SFTSV IgG antibodies can persist for up to 14 years. [ABSTRACT FROM AUTHOR]