Our results that human neutrophils bind low levels of IFN-λ3 and express low levels of IFN-λR1 are in contrast to mouse models of influenza virus or Aspergillus fumigatus infection and arthritis or colitis where mouse neutrophils directly respond to IFN-λ to modulate responses [19, 20, 25, 46]. This evidence concerns the gene IFNLR1 and arthritic joint disease.