Author: McCarthy, Mary K.; Reynoso, Glennys V.; Winkler, Emma S.; Mack, Matthias; Diamond, Michael S.; Hickman, Heather D.; Morrison, Thomas E.
Title: MyD88-dependent influx of monocytes and neutrophils impairs lymph node B cell responses to chikungunya virus infection via Irf5, Nos2 and Nox2 Document date: 2020_1_30
ID: 1tut4erh_32
Snippet: Type I IFNs can promote monocyte recruitment during inflammatory responses [5, 50] . Our data reveal distinct roles for IFNAR1, MyD88, and IL-1R in the recruitment of monocytes and neutrophils to the dLN. Neutrophil recruitment was inhibited by IFNAR1 signaling, but required IL-1R-MyD88 signaling. These findings agree with prior reports demonstrating IL-1R-dependent neutrophil recruitment in response to several inflammatory stimuli [51] [52] [53].....
Document: Type I IFNs can promote monocyte recruitment during inflammatory responses [5, 50] . Our data reveal distinct roles for IFNAR1, MyD88, and IL-1R in the recruitment of monocytes and neutrophils to the dLN. Neutrophil recruitment was inhibited by IFNAR1 signaling, but required IL-1R-MyD88 signaling. These findings agree with prior reports demonstrating IL-1R-dependent neutrophil recruitment in response to several inflammatory stimuli [51] [52] [53] , and a single report showing IFNAR1-mediated inhibition of neutrophil recruitment to inflamed lungs following influenza A virus infection [54] . In contrast to neutrophils, monocyte recruitment to the dLN following pathogenic CHIKV infection was independent of IFNAR1 and IL-1R signaling. However, the percentage and number of monocytes in the dLN was reduced in MyD88-deficient mice, indicating that one or more TLRs likely drive monocyte recruitment.
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