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- W4313368624 abstract "Abstract The non-physiological phenomenon whereby macrophages phagocytose healthy host cells is a hallmark of severe inflammatory disorders such as hemophagocytic lymphohistiocytosis (HLH). The mechanisms underlying the nascence of hemophagocytic macrophages, however, remain largely unknown. Under healthy conditions, macrophages are non-hemophagocytic and therefore do not eat healthy host cells, owing to the inhibitory myeloid receptor SIRPα. However, we previously showed that, unless inflammatory stimulation via TLR agonists or certain pro-inflammatory cytokines is also provided, the mere absence of SIRPα does not drive macrophages to become hemophagocytic. Here we show that hemophagocytic macrophages may arise under inflammatory conditions given an absence of SIRPα signaling and thereby lead to a severe inflammatory state reminiscent of HLH. SIRPα-knockout (Sirpα−/−) mice injected with the TLR9 agonist CpG rapidly developed characteristics of HLH, e.g., hemophagocytosis, anemia, thrombocytopenia, leukopenia, hepatosplenomegaly, hyperferritinemia, hypertriglyceridemia, and hypercytokinemia, with much greater severity than wild-type mice. Interestingly, IFNγ, a putative driver of HLH, was dispensable in the immunopathology of TLR9-driven HLH in Sirpα−/− mice, as IFNγ neutralization did not ameliorate any symptoms of HLH. As with CpG, other TLR agonists (Poly I:C, LPS, Zymosan) or cytokines (TNFα, IL-6, IL-17A) induced hemophagocytic macrophages that incurred severe HLH in Sirpα−/− mice. Together, these findings implicate that a pre-disposing loss of SIRPα signaling under inflammatory conditions may give rise to hemophagocytic macrophages that drive an HLH-like disease independent of IFNγ." @default.
- W4313368624 created "2023-01-06" @default.
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- W4313368624 date "2020-05-01" @default.
- W4313368624 modified "2023-09-27" @default.
- W4313368624 title "Absence of SIRPα signaling drives TLR9-induced hemophagocytic lymphohistiocytosis-like disease independent of IFN-γ in mice" @default.
- W4313368624 doi "https://doi.org/10.4049/jimmunol.204.supp.145.5" @default.
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