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Chronic restraint stress promotes lymphocyte apoptosis by modulating CD95 expression
1Department of Immunology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.
The Journal of Experimental Medicine
|April 19, 2000
Summary
Chronic stress significantly reduces splenocytes in mice via CD95-mediated apoptosis, involving endogenous opioids but not the hypothalamo-pituitary-adrenal axis. This immune suppression mechanism is crucial for understanding stress impacts.
Area of Science:
- Immunology
- Neuroscience
- Stress Physiology
Background:
- Stress impacts the immune system, but the precise mechanisms are not fully understood.
- Hormonal and neurotransmitter alterations are known effects of stress on the body.
Purpose of the Study:
- To elucidate the mechanisms by which chronic stress affects immune cell populations.
- To investigate the role of CD95 (Fas/APO-1) and endogenous opioids in stress-induced immune changes.
Main Methods:
- Mice were subjected to chronic physical restraint stress.
- Splenocyte apoptosis was assessed using TUNEL assay.
- CD95 expression and ligand interactions were analyzed.
- Opioid receptor antagonists (naltrexone, naloxone) and Fas-blocking agents were used.
- Experiments were conducted in adrenalectomized and CD95-deficient mice.
Main Results:
- Chronic stress led to a significant reduction in splenocytes, mediated by apoptosis.
- CD95 expression increased on splenic lymphocytes following stress.
- Stress-induced lymphocyte reduction was blocked by Fas-blocking agents and opioid antagonists.
- The effect was independent of the hypothalamo-pituitary-adrenal axis and absent in CD95-deficient mice.
Conclusions:
- Stress modulates the immune system through CD95-mediated apoptosis.
- Endogenous opioids play a critical role in this stress response pathway.
- The hypothalamo-pituitary-adrenal axis is not the primary mediator of this specific stress-induced immune suppression.