Abstract:
:Here, we examine the mechanism by which plasmacytoid dendritic cells (pDCs) and type I interferons promote humoral autoimmunity. In an amyloid-induced experimental autoimmune model, neutrophil depletion enhanced anti-nuclear antibody development, which correlated with heightened IFN-γ production by natural killer (NK) cells. IFN-α/β produced by pDCs activated NK cells via IL-15 induction. Neutrophils released reactive oxygen species (ROS), which negatively modulated the levels of IL-15, thereby inhibiting IFN-γ production. Mice deficient in NADPH oxidase 2 produced increased amounts of IFN-γ and developed augmented titers of autoantibodies. Both the pDC-IFN-α/β pathway and IFN-γ were indispensable in stimulating humoral autoimmunity. Male NZB/W F1 mice expressed higher levels of superoxide than their female lupus-prone siblings, and depletion of neutrophils resulted in spontaneous NK cell and autoimmune B cell activation. Our findings suggest a regulatory role for neutrophils in vivo and highlight the importance of an NK-IFN-γ axis downstream of the pDC-IFN-α/β pathway in systemic autoimmunity.
journal_name
Cell Repjournal_title
Cell reportsauthors
Huang X,Li J,Dorta-Estremera S,Di Domizio J,Anthony SM,Watowich SS,Popkin D,Liu Z,Brohawn P,Yao Y,Schluns KS,Lanier LL,Cao Wdoi
10.1016/j.celrep.2015.07.021subject
Has Abstractpub_date
2015-08-18 00:00:00pages
1120-32issue
7issn
2211-1247pii
S2211-1247(15)00761-5journal_volume
12pub_type
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