ArticleNature communications2023
Langerhans cells shape postnatal oral homeostasis in a mechanical-force-dependent but microbiota and IL17-independent manner.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Distinct postnatal trajectories of mouse dendritic epidermal T cells and Langerhans cells independent of microbiota.Science advances · 2026Article
- Maternal antibodies regulate the establishment of murine oral and salivary mucosal immunity.Nature communications · 2026Article
- Gingival spatial analysis reveals geographic immunological variation in a microbiota-dependent and -independent manner.NPJ biofilms and microbiomes · 2024Article
- Epithelial RANKL Limits Experimental Periodontitis via Langerhans Cells.Journal of dental research · 2024Article
- The role of the epithelial sentinels, Langerhans cells and γδT cells, in oral squamous cell carcinoma.Periodontology 2000 · 2024Review
- Convergent evolution of monocyte differentiation in adult skin instructs Langerhans cell identity.Science immunology · 2024Article
- An update on periodontal inflammation and bone loss.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The postnatal interaction between microbiota and the immune system establishes lifelong homeostasis at mucosal epithelial barriers, however, the barrier-specific physiological activities that drive the equilibrium are hardly known. During weaning, the oral epithelium, which is monitored by Langerhans cells (LC), is challenged by the development of a microbial plaque and the initiation of masticatory forces capable of damaging the epithelium. Here we show that microbial colonization following birth facilitates the differentiation of oral LCs, setting the stage for the weaning period, in which 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 naturally occurring alveolar bone loss. Mechanistically, masticatory forces induce the migration of LCs to the lymph nodes, and in return, LCs support the development of immunity to maintain epithelial integrity in a microbiota-independent manner. Unlike in adult life, this bone loss is IL-17-independent, suggesting that the establishment of oral mucosal homeostasis after birth and its maintenance in adult life involve distinct mechanisms.
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