IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system | Proceedings of the National Academy of Sciences thumbnail
IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system | Proceedings of the National Academy of Sciences
www.pnas.org
atients with relapsing–remitting multiple sclerosis (RRMS) have an increased frequency of IL-11+ monocytes, IL-11+ and IL-11R+ CD4+ lymphocytes, and IL-11R+ neutrophils in comparison to matched healthy controls. IL-11+ and granulocyte-macrophage colony-stimulating factor (GM-CSF)+ monocytes, CD4+ ly
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  • atients with relapsing–remitting multiple sclerosis (RRMS) have an increased frequency of IL-11+ monocytes, IL-11+ and IL-11R+ CD4+ lymphocytes, and IL-11R+ neutrophils in comparison to matched healthy controls.
  • IL-11+ and granulocyte-macrophage colony-stimulating factor (GM-CSF)+ monocytes, CD4+ lymphocytes, and neutrophils accumulate in the cerebrospinal fluid (CSF).
  • Previous reports on GM-CSF-regulated IL-1β monocyte secretion proposed IL-1β as a key mediator of the inflammatory cell migration across the blood–brain barrier (BBB) (3, 4). However, the role of IL-11 and NLRP3 inflammasome activation in inducing IL-1β+ monocyte migration in MS has not been elucidated.
  • genes involved in cell migration (CD81, VEGFA, and VEGFB).
  • RREAE mice following αIL-11 mAb treatment. αIL-11 mAb decreased the gene expression of NFKB, NLRP3, IL1B, and VEGFA in sorted IL-11R+ Ly6C+ monocytes, and the numbers of TLR7+, NFκB p65+, NLRP3+, and IL-1b+ monocytes in the CNS infiltrates of treated mice,

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