CSF2 and infection: Other studies have revealed that antibody blockade or genetic deletion of GM-CSF ameliorates colitis induced by the transfer of naïve T cells, infection with Helicobacter hepaticas, and administration of anti-CD40 agonistic antibodies [55, 76, 77], suggesting a highly pathogenic role of GM-CSF in targeting the differentiation of granulocyte‒myeloid progenitors (GMPs) and their effector functions [76].