Langerhans cells shape postnatal oral homeostasis in a mechanical force-dependent but microbiota and IL17-independent manner
The postnatal microbiota-immune axis establishes lifelong homeostasis at mucosal epithelial barriers. However, whether barrier-specific physiological activities regulate this process remains ill-defined. During weaning, the oral epithelium, which is monitored by Langerhans cells (LCs), is challenged by the development of a microbial plaque and the initiation of masticatory forces capable of damaging the epithelium. We demonstrate that microbial colonization following birth facilitates the differentiation of oral LCs, setting the stage for the weaning period, where adaptive immunity develops. Despite the presence of the challenging microbial plaque, LCs mainly respond to masticatory mechanical forces, inducing adaptive immunity to maintain epithelial integrity that is also associated with bone loss. Unlike adult life, this bone loss is IL-17-independent, suggesting that the establishment and maintenance of oral mucosal homeostasis involve distinct mechanisms. Moreover, barrier-specific features play a fundamental role in this early-life process. Overall design: the samples are mice gingival epithelium samples taken from Langerin-DTR mice that were injected with either PBS or Diphtheria toxin, and therefore are either depleted (DT) or non depleted (PBS) of Langerhans cells. The samples include 5 replicates of PBS samples and 6 replicates of DT samples.