Data from: Mouse gingival single cell transcriptomic atlas identified a novel fibroblast subpopulation activated to guide oral barrier immunity in periodontitis

Periodontitis, one of the most common non-communicable diseases, is
characterized by chronic oral inflammation and uncontrolled tooth
supporting alveolar bone resorption. Its underlying mechanism to initiate
aberrant oral barrier immunity has yet to be delineated. Here, we report a
unique fibroblast subpopulation activated to guide oral inflammation (AG
fibroblasts) identified in a single-cell RNA sequencing gingival cell
atlas constructed from the mouse periodontitis models. AG fibroblasts
localized beneath the gingival epithelium and in the cervical periodontal
ligament responded to the ligature placement and to the discrete topical
application of Toll-like receptor stimulants to mouse maxillary tissue.
The upregulated chemokines and ligands of AG fibroblasts linked to the
putative receptors of neutrophils in the early stages of periodontitis. In
the established chronic inflammation, neutrophils together with AG
fibroblasts appeared to induce type 3 innate lymphoid cells (ILC3s) that
were the primary source of interleukin-17 cytokines. The comparative
analysis of Rag2-/- and Rag2gc-/- mice suggested that ILC3 contributed to
the cervical alveolar bone resorption interfacing the gingival
inflammation. We propose that the AG fibroblast–neutrophil–ILC3 axis as a
previously unrecognized mechanism which could be involved in the complex
interplay between oral barrier immune cells contributing to pathological
inflammation in periodontitis.