IL10RA and infection: Whereas anti–IL-10R mAb treatment failed to significantly increase the numbers of any of the examined splenic innate populations during primary or secondary infection, including red pulp macrophages (the numbers of which were comparable in primary- and secondary-infected mice [Fig. 6C]), anti–IL-10R significantly elevated the expression of MHC II by inflammatory monocytes during both primary and secondary infections, and by red pulp macrophages and dendritic cells specifically during primary infection (Fig. 6D).