Abstract

Innate lymphoid cells (ILCs) are emerging as important players in inflammatory diseases. The oral mucosal barrier harbors all ILC subsets, but how these cells regulate the immune responses in periodontal ligament tissue during periodontitis remains undefined. Here, we show that total ILCs are markedly increased in periodontal ligament of periodontitis patients compared with healthy controls. Among them, ILC1s and ILC3s, particularly NKp44+ILC3 subset, are the predominant subsets accumulated in the periodontal ligament. Remarkably, ILC1s and ILC3s from periodontitis patients produce more IL-17A and IFN-γ than that from healthy controls. Collectively, our results highlight the role of ILCs in regulating oral immunity and periodontal ligament inflammation and provide insights into targeting ILCs for the treatment of periodontitis.

Highlights

  • Periodontitis is a common chronic inflammatory disease characterized by oral mucosal tissue destructive inflammation, which leads to periodontal ligament damage, loss of supporting bone, and tooth loss [1, 2]

  • Innate lymphoid cells (ILCs) Are Increased in Periodontal Ligament of Periodontitis Patients

  • ILC2s are defined by the expression of CRTH2, ILC3s are classified by the expression of CD117

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Summary

Introduction

Periodontitis is a common chronic inflammatory disease characterized by oral mucosal tissue destructive inflammation, which leads to periodontal ligament damage, loss of supporting bone, and tooth loss [1, 2]. Microbial dysbiosis is thought to be the trigger of the oral soft tissue inflammation and current standard of care largely rely on the removal of microbial biofilm by mechanical removal or antibiotics [3]. Innate lymphoid cells (ILCs) are a recently identified family of tissue-resident lymphocytes that lack adaptive antigen receptors. ILCs mainly reside at mucosal barrier surfaces that are able to provide an immediate immune response with rapid cytokines secretion in response to environmental stimuli [6]. ILCs play important roles in regulating inflammation, immunity, tissue repair, and homeostasis

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