Skin epidermal Langerhans cells (LCs) originate from embryonic precursors that self-renew locally at steady state. In Immunity, Capucha et al. show that in contrast to that, a large percentage of LCs in the oral mucosa derive from circulating progenitors under steady-state conditions. LCs appear in the oral mucosa 1 week after birth. In contrast to skin LCs, which are radioresistant and remain of host origin in parabiotic mice, a large percentage of oral mucosa LCs are donor derived in bone marrow–chimeric mice (50%) or parabiotic mice (20%), and they proliferate faster than epidermal LCs do after depletion of dendritic cells (DCs). Similar to conventional DCs, oral LCs derive from common DC and pre-DC progenitors, which contribute mostly to CD103+CD11b− LCs and less to CD103−CD11b+ LCs in the oral mucosa, whereas a fraction of the CD11b+ oral LCs originate from monocytes. In addition to the more dynamic homeostasis, the transcriptomic signatures and function of oral mucosa LCs resemble those of skin LCs.

Immunity (28 July 2015) doi:10.1016/j.immuni.2015.06.017