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Peer-reviewedCC BYJournal of Clinical Investigation

Immune responses in aging adults

  • Cornelia M. Weyand1,2,3,4
  • Jörg J. Goronzy2,3,4
4 affiliations
  1. 1Department of Cardiovascular Medicine, Mayo Clinic Alix School of Medicine, Rochester, Minnesota, USA
  2. 2Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA
  3. 3Department of Medicine and
  4. 4Stanford University School of Medicine, Stanford, California, USA
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Abstract

As a widely distributed network of cells, tissues, and organs, the human immune system is profoundly vulnerable to the effects of aging. Intrinsic and extrinsic stressors progressively erode its structural integrity and functional resilience, weakening core protective responses and increasing susceptibility to infection, malignancy, and tissue degeneration. At the same time, aging heightens the risk of chronic inflammation and autoimmune disease. Hematopoietic stem cells become uniquely compromised as aging intensifies metabolic and replicative stress. Their continuous high-volume turnover results in diminished self-renewal capacity, skewed lineage output, and dominance of expanded clones. These changes undermine innate immune competence and amplify inflammatory activity. Adaptive immune function declines with age through coordinated cellular and molecular programs. T and B lymphocytes exhibit a decline in naive cells, progressive loss of stemness, shortened lifespan, and constrained clonal diversity. Aging lymphocytes reconfigure transcriptional networks, undergo widespread organelle dysfunction, develop maladaptive stress responses, and redistribute into noncanonical tissue niches. Collectively, these alterations reduce antigen specificity and precision, promote innate-like immune behavior, and confer resistance to tolerance. These mechanisms result in concurrent immunodeficiency and autoimmunity, exemplified by two autoimmune diseases disproportionately affecting older adults: rheumatoid arthritis and giant cell arteritis.

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Cite

BibTeXRIS
BibTeX
@article{weyand2026immune,
  title = {{Immune responses in aging adults}},
  author = {Cornelia M. Weyand and Jörg J. Goronzy},
  journal = {Journal of Clinical Investigation},
  year = {2026},
  month = jun,
  doi = {10.1172/jci206227},
  url = {https://doi.org/10.1172/jci206227},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Immune responses in aging adults
AU  - Cornelia M. Weyand
AU  - Jörg J. Goronzy
PY  - 2026
DA  - 2026/06/14
JO  - Journal of Clinical Investigation
DO  - 10.1172/jci206227
UR  - https://doi.org/10.1172/jci206227
AB  - As a widely distributed network of cells, tissues, and organs, the human immune system is profoundly vulnerable to the effects of aging. Intrinsic and extrinsic stressors progressively erode its structural integrity and functional resilience, weakening core protective responses and increasing susceptibility to infection, malignancy, and tissue degeneration. At the same time, aging heightens the risk of chronic inflammation and autoimmune disease. Hematopoietic stem cells become uniquely compromised as aging intensifies metabolic and replicative stress. Their continuous high-volume turnover results in diminished self-renewal capacity, skewed lineage output, and dominance of expanded clones. These changes undermine innate immune competence and amplify inflammatory activity. Adaptive immune function declines with age through coordinated cellular and molecular programs. T and B lymphocytes exhibit a decline in naive cells, progressive loss of stemness, shortened lifespan, and constrained clonal diversity. Aging lymphocytes reconfigure transcriptional networks, undergo widespread organelle dysfunction, develop maladaptive stress responses, and redistribute into noncanonical tissue niches. Collectively, these alterations reduce antigen specificity and precision, promote innate-like immune behavior, and confer resistance to tolerance. These mechanisms result in concurrent immunodeficiency and autoimmunity, exemplified by two autoimmune diseases disproportionately affecting older adults: rheumatoid arthritis and giant cell arteritis.
SN  - 0021-9738
SN  - 1558-8238
ER  -