News

Social stress can speed up immune system aging

Eric Klopack
By Eric Klopack
July 2, 2022

As people age, their immune systems naturally begin to decline. This aging of the immune system, called immunosenescence, may be an important part of such age-related health problems as cancer and cardiovascular disease, as well as older people’s less effective response to vaccines.

But not all immune systems age at the same rate. In our recently published study, my colleagues and I found that social stress is associated with signs of accelerated immune system aging.

Stress and immunosenescence

To better understand why people with the same chronological age can have different immunological ages, my colleagues and I looked at data from the Health and Retirement Study, a large, nationally representative survey of U.S. adults over age 50. HRS researchers ask participants about different kinds of stressors they have experienced, including stressful life events, such as job loss; discrimination, such as being treated unfairly or being denied care; major lifetime trauma, such as a family member’s having a life-threatening illness; and chronic stress, such as financial strain.

Recently, HRS researchers have also started collecting blood from a sample of participants, counting the number of different types of immune cells present, including white blood cells. These cells play a central role in immune responses to viruses, bacteria and other invaders. This is the first time such detailed information about immune cells has been collected in a large national survey.

As people age, the T cells in the immune systems become less effective at fighting pathogens.
As people age, the T cells in the immune systems become less effective at fighting
pathogens.

By analyzing the data from 5,744 HRS participants who both provided blood and answered survey questions about stress, my research team and I found that people who experienced more stress had a lower proportion of “naive” T cells – fresh cells needed to take on new invaders the immune system hasn’t encountered before. They also have a larger proportion of “late differentiated” T cells – older cells that have exhausted their ability to fight invaders and instead produce proteins that can increase harmful inflammation. People with low proportions of newer T cells and high proportions of older T cells have a more aged immune system.

After we controlled for poor diet and low exercise, however, the connection between stress and accelerated immune aging wasn’t as strong. This suggests that improving these health behaviors might help offset the hazards associated with stress.

Similarly, after we accounted for potential exposure to cytomegalovirus – a common, usually asymptomatic virus known to accelerate immune aging – the link between stress and immune cell aging was reduced. While CMV normally stays dormant in the body, researchers have found that stress can cause CMV to flare up and force the immune system to commit more resources to control the reactivated virus. Sustained infection control can use up naive T cell supplies and result in more exhausted T cells that circulate throughout the body and cause chronic inflammation, an important contributor to age-related disease.

Email Twitter45 Facebook275 LinkedIn Print  As people age, their immune systems naturally begin to decline. This aging of the immune system, called immunosenescence, may be an important part of such age-related health problems as cancer and cardiovascular disease, as well as older people’s less effective response to vaccines.  But not all immune systems age at the same rate. In our recently published study, my colleagues and I found that social stress is associated with signs of accelerated immune system aging. Stress and immunosenescence  To better understand why people with the same chronological age can have different immunological ages, my colleagues and I looked at data from the Health and Retirement Study, a large, nationally representative survey of U.S. adults over age 50. HRS researchers ask participants about different kinds of stressors they have experienced, including stressful life events, such as job loss; discrimination, such as being treated unfairly or being denied care; major lifetime trauma, such as a family member’s having a life-threatening illness; and chronic stress, such as financial strain.  Recently, HRS researchers have also started collecting blood from a sample of participants, counting the number of different types of immune cells present, including white blood cells. These cells play a central role in immune responses to viruses, bacteria and other invaders. This is the first time such detailed information about immune cells has been collected in a large national survey. Read news coverage based on evidence, not tweets Scanning electron microscope image of a human T cell As people age, the T cells in the immune systems become less effective at fighting pathogens. National Institute of Allergy and Infectious Diseases/Flickr, CC BY-NC  By analyzing the data from 5,744 HRS participants who both provided blood and answered survey questions about stress, my research team and I found that people who experienced more stress had a lower proportion of “naive” T cells – fresh cells needed to take on new invaders the immune system hasn’t encountered before. They also have a larger proportion of “late differentiated” T cells – older cells that have exhausted their ability to fight invaders and instead produce proteins that can increase harmful inflammation. People with low proportions of newer T cells and high proportions of older T cells have a more aged immune system.  After we controlled for poor diet and low exercise, however, the connection between stress and accelerated immune aging wasn’t as strong. This suggests that improving these health behaviors might help offset the hazards associated with stress.  Similarly, after we accounted for potential exposure to cytomegalovirus – a common, usually asymptomatic virus known to accelerate immune aging – the link between stress and immune cell aging was reduced. While CMV normally stays dormant in the body, researchers have found that stress can cause CMV to flare up and force the immune system to commit more resources to control the reactivated virus. Sustained infection control can use up naive T cell supplies and result in more exhausted T cells that circulate throughout the body and cause chronic inflammation, an important contributor to age-related disease. Electron microscope image of cytomegalovirus visions After an initial infection, cytomegalovirus stays in the body for life.
After an initial infection, cytomegalovirus stays in the body for life.

Understanding immune aging

Our study helps clarify the association between social stress and faster immune aging. It also highlights potential ways to slow down immune aging, such as changing how people cope with stress and improving lifestyle behaviors like diet, smoking and exercise. Developing effective cytomegalovirus vaccines may also help alleviate immune system aging.

It is important to note, however, that epidemiological studies cannot completely establish cause and effect. More research is needed to confirm whether stress reduction or lifestyle changes will lead to improvements in immune aging, and to better understand how stress and latent pathogens like cytomegalovirus interact to cause illness and death. We are currently using additional data from the Health and Retirement Study to examine how these and other factors like childhood adversity affect immune aging over time.

Less aged immune systems are better able to fight infections and generate protective immunity from vaccines. Immunosenescence may help explain why people are likely to have more severe cases of COVID-19 and a weaker response to vaccines as they age. Understanding what influences immune aging may help researchers better address age-related disparities in health and illness.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The Conversation

Enjoy reading ASBMB Today?

Become a member to receive the print edition four times a year and the digital edition monthly.

Learn more
Eric Klopack
Eric Klopack

Eric Klopack is a postdoctoral researcher of gerontology at the University of Southern California.

Get the latest from ASBMB Today

Enter your email address, and we’ll send you a weekly email with recent articles, interviews and more.

Latest in Science

Science highlights or most popular articles

Training AI to uncover novel antimicrobials
Feature

Training AI to uncover novel antimicrobials

Oct. 9, 2025

Antibiotic resistance kills millions, but César de la Fuente’s lab is fighting back. By pairing AI with human insight, researchers are uncovering hidden antimicrobial peptides across the tree of life with a 93% success rate against deadly pathogens.

AI-designed biomarker improves malaria diagnostics
Journal News

AI-designed biomarker improves malaria diagnostics

Oct. 8, 2025

Researchers from the University of Melbourne engineered Plasmodium vivax diagnostic protein with enhanced yield and stability while preserving antibody-binding, paving the way for more reliable malaria testing.

Matrix metalloproteinase inhibitor reduces cancer invasion
Journal News

Matrix metalloproteinase inhibitor reduces cancer invasion

Oct. 8, 2025

Scientists at the Mayo Clinic engineered a TIMP-1 protein variant that selectively inhibits MMP-9 and reduces invasion of triple-negative breast cancer cells, offering a promising tool for targeted cancer research.

Antibiotic sensor directly binds drug in resistant bacteria
Journal News

Antibiotic sensor directly binds drug in resistant bacteria

Oct. 8, 2025

Researchers at Drexel University uncover how the vancomycin-resistant bacterial sensor binds to the antibiotic, offering insights to guide inhibitor design that restores antibiotic effectiveness against hospital-acquired infections.

ApoA1 reduce atherosclerotic plaques via cell death pathway
Journal News

ApoA1 reduce atherosclerotic plaques via cell death pathway

Oct. 1, 2025

Researchers show that ApoA1, a key HDL protein, helps reduce plaque and necrotic core formation in atherosclerosis by modulating Bim-driven macrophage death. The findings reveal new insights into how ApoA1 protects against heart disease.

Omega-3 lowers inflammation, blood pressure in obese adults
Journal News

Omega-3 lowers inflammation, blood pressure in obese adults

Oct. 1, 2025

A randomized study shows omega-3 supplements reduce proinflammatory chemokines and lower blood pressure in obese adults, furthering the understanding of how to modulate cardiovascular disease risk.