mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases

Front Immunol. 2022 Feb 10:13:827461. doi: 10.3389/fimmu.2022.827461. eCollection 2022.

Abstract

Periodontal disease results from the inflammatory infiltration by the microbial community which is marked through tooth mobility and alveolar bone resorption. The inflammation in periodontal disease is mediated by CD4+ T cells through cytokine secretion and osteoclastogenetic activity. Historically, the inflammatory model in periodontal disease is described through disruption of the balance between two subsets of T helper cells which are T-helper type 1 (Th1) and T-helper type 2 (Th2). However, more and more studies have found that apart from subsets of helper T cells, regulatory T-cells and Th17 cells are also involved in the pathogenesis of periodontal diseases. Growing evidence proves that helper T cells differentiation, activation, and subset determination are under the strong impact of mTOR signaling. mTOR signaling could promote Th1 and Th17 cell differentiation and inhibit Treg commitment through different mTOR complexes, therefore we anticipate a regulation effect of mTOR signaling on periodontal diseases by regulating CD4+ T cell subsets. This review aims to integrate the topical researches about the role of different types of Th cells in the pathogenesis of periodontal diseases, as well as the regulation of mTOR signaling in the specification and selection of Th cell commitment.

Keywords: CD4+ T cells; immune response; inflammatory; mTOR signaling; periodontal disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • CD4-Positive T-Lymphocytes* / metabolism
  • Humans
  • Periodontal Diseases* / metabolism
  • T-Lymphocyte Subsets / metabolism
  • TOR Serine-Threonine Kinases / metabolism
  • Th17 Cells

Substances

  • MTOR protein, human
  • TOR Serine-Threonine Kinases