Decrease of CD4(+)FOXP3(+) T regulatory cells in the peripheral blood of human subjects undergoing a mental stressor

Area of Science:

• Immunology
• Neuroendocrinology
• Stress Research

Background:

• Acute psychological stress activates the adaptive immune response, increasing effector T cells.
• T regulatory cells (Tregs) are vital for maintaining self-tolerance and preventing autoimmunity.
• The impact of stress on Treg behavior within the adaptive immune response was previously unexamined.

Purpose of the Study:

• To investigate the dynamic changes in T regulatory cells (Tregs) under acute psychological stress.
• To analyze the expression of Treg-related molecules and stress receptors on T cells.
• To understand the implications of stress-induced immune alterations for autoimmune conditions.

Main Methods:

• Utilized a crossover design with 31 healthy males undergoing a laboratory stressor and serving as their own controls.
• Employed flow cytometry to quantify T cell subpopulations, including CD4(+)FOXP3(+) Tregs.
• Analyzed the expression of cytotoxic T-lymphocyte antigen-4 (CTLA-4), latency associated peptide (LAP), and stress hormone receptors (beta(1)-adrenergic, glucocorticoid alpha) on peripheral T cells.

Main Results:

• Confirmed previous findings of decreased naïve and central memory T cells post-stress.
• Demonstrated a significant decrease in CD4(+)FOXP3(+) Tregs during acute psychological stress.
• Observed reduced expression of CTLA-4 and LAP in Tregs and overexpression of beta(1)-adrenergic and glucocorticoid alpha receptors on Tregs.

Conclusions:

• Acute psychological stress leads to a downregulation of T regulatory cells (Tregs), key inhibitors of immune responses.
• Stress-induced Treg reduction, particularly with chronic stress, could exacerbate inflammatory and autoimmune diseases.
• Tregs may be particularly sensitive to stress via beta(1)-adrenergic and glucocorticoid alpha receptors, mediating immune modulation.