Plasticity of T helper cell subsets: Implications in periodontal disease

Abstract

T helper (Th) cells have an important role in host defence as well in the pathogenesis of periodontal disease. Th cells differentiate from naive cells into various subsets, each of which is associated with a set of inducing and effector cytokines. Previously, it was thought that this differentiation was an irreversible event. Recent evidence suggest that even differentiated Th cells, retain the flexibility to transform from one lineage to another, a phenomenon referred to as plasticity. This plasticity is thought to be brought about by epigenetic modifications that are regulated by external and internal signals in the micro-environment of these cells. The factors and mechanisms which affect the plasticity of these cells and their potential role in the etio-pathogenesis of periodontal disease has been described in this article.

Keywords: Epigenetic modification; T helper cell; periodontal disease; plasticity.

Figure 1

Epigenetic Modification. Histone deacetylation causes the condensation of chromatin, making it inaccessible to transcription factors and the genes are therefore silenced. Chromatin containing acetylated histones (histone acetylation) are open and accessible to transcription factors and the genes are potentially active. This modification may be associated with deoxyribonucleic acid (DNA) methylation. DNA methylation involves methylation of cytosine-phosphate-guanosine islands at the promoter region, directly switching off gene expression by preventing transcription factors from binding to the promoter region

Figure 2

Cytokine regulation of epigenetic modifications and T helper cell plastiticty