CD4⁺T cell activation and associated susceptibility to HIV‐1 infection in vitro increased following acute resistance exercise in human subjects

Abstract

Early studies in exercise immunology suggested acute bouts of exercise had an immunosuppressive effect in human subjects. However, recent data, show acute bouts of combined aerobic and resistance training increase both lymphocyte activation and proliferation. We quantified resistance exercise‐induced changes in the activation state of CD4+ T lymphocytes via surface protein expression and using a medically relevant model of infection (HIV‐1). Using a randomized cross‐over design, 10 untrained subjects completed a control and exercise session. The control session consisted of 30‐min seated rest while the exercise session entailed 3 sets × 10 repetitions of back squat, leg press, and leg extensions at 70% 1‐RM with 2‐min rest between each set. Venous blood samples were obtained pre/post each session. CD4+ T lymphocytes were isolated from whole blood by negative selection. Expression of activation markers (CD69 & CD25) in both nonstimulated and stimulated (costimulation through CD3+CD28) cells were assessed by flow cytometry. Resistance exercised‐induced effects on intracellular activation was further evaluated via in vitro infection with HIV‐1. Nonstimulated CD4+ T lymphocytes obtained postexercise exhibited elevated CD25 expression following 24 h in culture. Enhanced HIV‐1 replication was observed in cells obtained postexercise. Our results demonstrate that an acute bout of resistance exercise increases the activation state of CD4+ T lymphocytes and results in a greater susceptibility to HIV‐1 infection in vitro. These findings offer further evidence that exercise induces activation of T lymphocytes and provides a foundation for the use of medically relevant pathogens as indirect measures of intracellular activation.

OX40L/OX40 Signal Promotes IL-9 Production by Mucosal MAIT Cells During Helicobacter pylori Infection

“…Since OX40 promoted IL-9 production of MAIT cells, we then examined whether OX40 facilitated MAIT cell activation in H. pylori -induced gastritis, as what we found in T2D patients ( 11 ). As expected, OX40 + MAIT cells from H. pylori gastritis patients were found to express high levels of CD69 and CD25 ( Figures 3A,B ), which are T cell activating markers ( 29 , 30 ). Meanwhile, a positive correlation was observed between the percentage of OX40 + T cells and MAIT cells ( Figure 3C ), indicating that OX40 may promote MAIT cell proliferation.…”

TLR7 Modulated T Cell Response in the Mesenteric Lymph Node of Schistosoma japonicum-Infected C57BL/6 Mice

“…These results suggested that S. japonicum infection could induce strong immune response in intestinal tract. CD25 and CD69 were classic markers for T cell activation [33], though CD4 + CD25 + foxp3 + T cells were served as nature regulatory T cells (Treg) [35], and CD69 was seem to be a marker for tissue resident memory T cells (TRM) [36]. Higher percentages of CD25 and CD69-expressing CD3 + T were found in the infected mouse MLN.…”

“…However, because of the number of MLN mononuclear cells in response to infection dramatically increased, the absolute number of MLN CD3 + T cells was obviously increased after infection (P < 0:05, Figure 1(e)). CD25 and CD69 were classic markers for T cell activation [33]. To detect the degree of activation, the expression of CD25 and CD69 on CD3 + T cells was detected by the cell surface staining.…”

High-intensity interval training in allogeneic adoptive T-cell immunotherapy – a big HIT?

“…Even though the difference between the two exercise protocols was not statistically significant, cholesterol levels and CD69 expression in CD8 + T cells increased significantly after continuous exercise, predominantly in moderately fit donors. As early marker for VSTs activation [61], the observed increases in CD69 and cholesterol correlated well with higher IFN-γ secretion. In a comprehensive future study, we will investigate the impact and modulatory role of cholesterol on VST activation and function.…”