Producing Trojans: hijacking of monocyte differentiation by pathogens

Pathogens can exploit the plasticity of host immune cells, such as the pathway of monocyte differentiation into macrophages and dendritic cells. This review discusses how microbial pathogens hijack the monocyte fate and reprogram macrophages to establish infection, evade immune surveillance, and persist within the host. Viruses such as HIV and cytomegalovirus (CMV) rewire host sentinel cells through modulation of transcriptional networks, cytokine signaling cascades, and autophagic pathways. Bacterial pathogens such as Mycobacterium tuberculosis, Salmonella enterica, or Bordetella pertussis create safe replication niches by disrupting monocyte differentiation. Fungal pathogens expand this repertoire by leveraging cytokine modulation and phenotypic reprogramming to subvert host innate and pathogen-specific immune responses. We highlight here the newly emerging molecular mechanisms of monocyte reprogramming towards pathogen survival and transmission.