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).