Myeloid expression of the AP‐1 transcription factor JUNB modulates outcomes of type 1 and type 2 parasitic infections

摘要: Summary Activation of macrophages is a key step in the initiation immune responses, but transcriptional mechanisms governing macrophage activation during infection are not fully understood. It was recently shown that AP-1 family transcription factor JUNB positively regulates response to Toll-like receptor agonists promote classical or M1 polarization, as well cytokine interleukin-4 (IL-4), which elicits an alternatively activated M2 phenotype. However, role for has never been demonstrated in vivo. Here, dissect physiological setting, mice lacking specifically myeloid cells were tested two models: experimental cerebral malaria, pathological type 1 response, and helminth infection, 2 responses protective. Myeloid-restricted deletion Junb reduced activation, associated with pathology improved survival Plasmodium berghei. Myeloid deficiency also compromised hookworm Nippostrongylus brasiliensis, leading diminished production eosinophil recruitment increased parasite burden. These results demonstrate shapes host outcomes infections.