H. polygyrus infection induced increase in blood monocytes and
lung mononuclear phagocytes is IFN-I signalling dependent.
IFN-I signalling through IFNAR is essential to the H. polygyrusinduced anti-viral effect6. To test if the expansion
in mononuclear phagocytes was dependent on this signalling axis, cell
counts were assessed 10 dpi with H. polygyrus inIfnar1–/– mice, which are maintained on a
C57BL/6 background. Importantly, the H. polygyrus induced
expansion of lung mononuclear phagocytes (Fig. 4A) and of circulatory
monocytes (Fig. 4B) were evident in control C57BL/6 mice but lost in the
absence of IFN-I signalling. In contrast, IFNAR-deficient mice still had
increases in committed monocyte progenitors in the bone marrow afterH. polygyrus , albeit to a lower level than in wild type controls.
Ly6C+ monocyte numbers in the bone marrow also seemed
to increase after H. polygyrus , but without reaching statistical
significance (Fig. 4C,D).