Objective: 

An effective immune response protects organism, differentiate self from non-self and terminate rapidly when threat disappears. Smooth functioning of the immune response, controlled by cytokinergic interactions of helper T (Th1, Th2&Th17) and regulatory T (Treg) cells, is crucial and modulated by stressors. Albeit the extensive studies on stress-immune system interactions, Th17 and Treg response to stress has not been investigated, yet. We aimed to determine the effect of acute or chronic stress on peripheral T lymphocyte distribution.

Methods: 

Male, Swiss-albino mice (30–40 g) were allocated in 3 groups as; control (n=11), acute stress (n=11) and chronic stress (n=11). Cold-immobilization stress was applied in a restrainer at 4°C once for 6 hours in acute stress group and 5 consecutive days for 6 hours/day for chronic stress group. In the blood samples withdrawn after stress protocols and corresponding times in control groups serum cortisol and cytokine levels (IL-2, IL-4, TNFa, IL-17) were measured and distribution of lymphocyte subgroups were determined flow-cytometrically.

Results: 

The effect of acute and chronic stress on distribution of T-lymphocyte subgroups was different. Chronic stress attenuated the number of Th17 and Treg cells more.

Conclusions: 

Stress is a key modulator of immune response altering the reaction of Th cells, chief executive officers of acquired immune system. Further insights about mutual interaction of Treg and Th17 cells will help better understanding of the pathogenesis and provide a new era in management of especially autoimmune diseases. This study is granted by HUBAB (Project number: 011 D04 101 003)