IL-17 and IFN-γ Productions by CD4+ T cells and T cell Subsets Expressing NKG2D Associated with the Number of Risk Factors for Cardiovascular Diseases

Traditional Thai Massage Promoted Immunity in the Elderly via Attenuation of Senescent CD4+ T Cell Subsets: A Randomized Crossover Study

“…In aging and immune disorders, increased aberrant CD4+CD28 null occurs [14,16,18,[22][23][24], with predominantly NKG2D expression [19,20,25,26]. Several studies have indicated that these senescent CD4+ T cells are associated with pathogenic features in chronic inflammatory diseases, including autoimmune diseases [18,19,22], cardiovascular diseases (CVD) [18,20], diabetes mellitus (DM) [26], and advanced age [16,18,[23][24][25]. These immunosenescence cells can also produce proinflammatory cytokines, such as IFN-γ, IL-6, TNF-α, and IL-17 [14,[18][19][20]26].…”

“…Several studies have indicated that these senescent CD4+ T cells are associated with pathogenic features in chronic inflammatory diseases, including autoimmune diseases [18,19,22], cardiovascular diseases (CVD) [18,20], diabetes mellitus (DM) [26], and advanced age [16,18,[23][24][25]. These immunosenescence cells can also produce proinflammatory cytokines, such as IFN-γ, IL-6, TNF-α, and IL-17 [14,[18][19][20]26]. Their presence may be linked to faster progression of age-related diseases.…”

“…Additionally, the effect of multiple rounds of TTM on subjects with high percentages of CD4+28 null NKG2D+ T cells was more evident than those in the low group. Activating receptor NKG2D of CD4+ T cells showed anomalous appearances, with rising expressions in chronic inflammation and autoimmunity [19,20,25,26]. The elderly with CD4+28 null NKG2D+ at more than 2.75% had significant decreases in their level of these cells after receiving multiple rounds of TTM.…”

“…All procedures are described elsewhere in previous studies [20,26]. The flow cytometry service was provided by the Research Instrument Center (RIC), Khon Kaen University, Thailand.…”

“…Normally, this cell type is activated via the signaling of T cell receptors (TCR) co-operating with a costimulatory molecule, CD28 [15]. In many conditions, such as chronic inflammations and infectious or autoimmune diseases [16][17][18][19][20], CD28 expressions were reduced or diminished (CD4+CD28 null ); however, surrogate co-stimulatory molecules were present on these cells, resulting in alterations in immune responses [14,16,18,[21][22][23][24]. Previous studies in the elderly suggested that the natural killer group 2 member D (NKG2D) played a role as one of the surrogate co-stimulatory molecules of CD4+CD28 null T cells, leading to higher pro-inflammatory cytokine production [16,[18][19][20][23][24][25][26].…”