Introduction
autoimmune diseases, articular damage, Rheumatoid arthritis, RA, autoimmune disease
DISEASE, AUTOIMMUNE DISEASES, RHEUMATOID ARTHRITIS, CHRONIC INFLAMMATION, AUTOIMMUNITY, PATHOGENESIS, AUTOIMMUNE DISEASE
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease of multifactorial origin that develops due to unfavorable coincidence of genetic, immune, and environmental factorsT helper 17 (Th17) and regulatory T cells (Treg cells) are both differentiated from the same naive CD4+ T cells, but in separate cytokine environments and with distinctive gene expression profilesAn aberrant Treg cell response with a shift towards a Th17 cell response characterizes the disease onset and course. The relationship between the imbalance of Th17/Treg cells and the production of pro- and anti-inflammatory cytokines is important for the onset and/or course of autoimmunity, chronic inflammation, and articular damage in the joints of RA patientsEpigenetic alterations like DNA methylation and histone acetylation accumulate with aging and provide a mechanistic link between immunosenescence and development of autoimmune diseases such as RA. T cell landscape is influenced by epigenetic mechanisms such as alteration in the global 5-methyl cytosine (5-mC) DNA, global 5-hydroxymethyl cytosine (5-hmC) DNA and histone deacetylase 1 (HDAC1) levels, which are susceptible to systemic factors, external stressors and environmental stimuliKeeping in mind the multifactorial etiology, diverse pathogenesis of RA, heterogeneous clinical phenotypes and the therapeutic potential of yoga, we hypothesized that yoga improves clinical outcome in RA by bringing changes in all interconnected biological components and at various levels—molecular, cellular, organ systems, and the person as a whole. With this novel context in mind, this study aimed to investigate the immune-modulatory effects of 8-weeks of yoga practice on disease severity, T cell sub-sets [Th17 (CD3+ CD4+ IL17+ RORγt+) cells and Treg (CD3+ CD4+ CD25+ CD127-Foxp3+) cells], markers of T cell aging [aged Th17 (CD3+ CD4+ IL17+ RORγt+ CD28−) cells and aged Treg (CD3+ CD4+ CD25+ CD127− Foxp3+ CD28−) cells], inflammatory markers [IL-6, IL-17, TGF-β, and IL-10], epigenetic alterations [5-mC, 5-hmC and HDAC1] and gene expression [