Involvement of JNK signaling in IL4-induced M2 macrophage polarization

•IL-4 induced high expression of JNK and transcription c-Myc in M2 macrophages.•JNK inhibition in M2 macrophages blocked c-Myc and led to an impaired M2 status.•JNK inhibition leads to the reduction of wound healing capacity of M2 cells.•M2 macrophages had high ability of migration depending on cytokines production.

It has been generally accepted that alternatively activated macrophages (M2), which can be induced by type 2 cytokines such as IL-4, is responsible for tissue repair. However, the function of JNK in IL-4-induced M2 macrophage polarization remains unclear. Here, we demonstrated that M0 macrophages can be polarized into M2 status in response to IL-4 stimulation with the increased expression of the M2-specific molecular markers. We also found that IL-4 induced higher expression of JNK and transcription factor c-Myc in M2 macrophages. Our Q-PCR and Western blot results showed that JNK increased the expression of c-Myc and M2 markers Arg1, Mrc1. We also demonstrated c-Myc was the downstream of IL-4-JNK pathway. Further, the depletion of c-Myc, Arg1 and Mrc1 could inhibit the migration ability of M2 macrophages. Taken together, our data establishes a new role for JNK signaling in IL-4-induced alternative activation of macrophages and may provide a novel strategy for immune therapy.