PMC:6710390 / 27128-28165 JSONTXT

{"project":"2_test","denotations":[{"id":"31481869-22272817-38391759","span":{"begin":127,"end":131},"obj":"22272817"},{"id":"31481869-16520005-38391760","span":{"begin":357,"end":361},"obj":"16520005"},{"id":"31481869-26988064-38391761","span":{"begin":537,"end":541},"obj":"26988064"},{"id":"31481869-23537508-38391762","span":{"begin":873,"end":877},"obj":"23537508"}],"text":"The sympathetic nervous system (SNS) is mechanically and functionally affected in both rheumatoid arthritis and MS (Sternberg, 2012). Clinical studies also suggested that the defective crosstalk between SNS and the immune system might further precipitate the manifestations of MS because of considerable SNS dysfunction in patients with MS (Shahabi et al., 2006). Substantial evidence indicated that stress can precipitate or worsen symptoms of inflammation in MS. NPY significantly promoted stress coping and resiliency (Wagner et al., 2016). Neuropeptides secreted under stress could activate microglia and mast cells to release inflammatory molecules. This results in the maturation and activation of Th17 autoimmune cells, destruction of the blood brain barrier (BBB), and T cells entering the CNS, which can promote brain inflammation and cause MS (Karagkouni et al., 2013). These indications give us clues to further investigate the role of NPY in regulating autoimmune processes and to identify a new therapeutic target of MS/EAE."}

{"project":"TEST0","denotations":[{"id":"31481869-127-135-481266","span":{"begin":127,"end":131},"obj":"[\"22272817\"]"},{"id":"31481869-223-231-481267","span":{"begin":357,"end":361},"obj":"[\"16520005\"]"},{"id":"31481869-72-80-481268","span":{"begin":537,"end":541},"obj":"[\"26988064\"]"},{"id":"31481869-218-226-481269","span":{"begin":873,"end":877},"obj":"[\"23537508\"]"}],"text":"The sympathetic nervous system (SNS) is mechanically and functionally affected in both rheumatoid arthritis and MS (Sternberg, 2012). Clinical studies also suggested that the defective crosstalk between SNS and the immune system might further precipitate the manifestations of MS because of considerable SNS dysfunction in patients with MS (Shahabi et al., 2006). Substantial evidence indicated that stress can precipitate or worsen symptoms of inflammation in MS. NPY significantly promoted stress coping and resiliency (Wagner et al., 2016). Neuropeptides secreted under stress could activate microglia and mast cells to release inflammatory molecules. This results in the maturation and activation of Th17 autoimmune cells, destruction of the blood brain barrier (BBB), and T cells entering the CNS, which can promote brain inflammation and cause MS (Karagkouni et al., 2013). These indications give us clues to further investigate the role of NPY in regulating autoimmune processes and to identify a new therapeutic target of MS/EAE."}

{"project":"0_colil","denotations":[{"id":"31481869-22272817-481266","span":{"begin":127,"end":131},"obj":"22272817"},{"id":"31481869-16520005-481267","span":{"begin":357,"end":361},"obj":"16520005"},{"id":"31481869-26988064-481268","span":{"begin":537,"end":541},"obj":"26988064"},{"id":"31481869-23537508-481269","span":{"begin":873,"end":877},"obj":"23537508"}],"text":"The sympathetic nervous system (SNS) is mechanically and functionally affected in both rheumatoid arthritis and MS (Sternberg, 2012). Clinical studies also suggested that the defective crosstalk between SNS and the immune system might further precipitate the manifestations of MS because of considerable SNS dysfunction in patients with MS (Shahabi et al., 2006). Substantial evidence indicated that stress can precipitate or worsen symptoms of inflammation in MS. NPY significantly promoted stress coping and resiliency (Wagner et al., 2016). Neuropeptides secreted under stress could activate microglia and mast cells to release inflammatory molecules. This results in the maturation and activation of Th17 autoimmune cells, destruction of the blood brain barrier (BBB), and T cells entering the CNS, which can promote brain inflammation and cause MS (Karagkouni et al., 2013). These indications give us clues to further investigate the role of NPY in regulating autoimmune processes and to identify a new therapeutic target of MS/EAE."}