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Immunosenescence: Aging at Its Crossroads 

As we age, our immune system declines, impacting B- and T-cell functions and causing chronic inflammation. A recent review by Snijckers & Foks in Frontiers in Immunology highlights these key points:


  • Aging shifts hematopoietic stem cells towards myelopoiesis, reducing lymphoid cell output from the bone marrow.

  • Thymic involution with age decreases peripheral naïve T cells while increasing memory T- and B cells.

  • B- and T-cell receptor diversity declines with age.

  • Aging impairs germinal center responses and deteriorates the structure and function of secondary lymphoid organs, disrupting T-B cell dynamics and increasing autoantibody production.

  • Aging induces cell cycle arrest, resistance to apoptosis, and a senescence-associated secretory profile.


These changes result in overall immune system decline, termed immunosenescence, and persistent low-grade inflammation, known as inflammaging. With an aging population, understanding maladaptive immune responses in atherosclerosis is crucial for developing targeted treatments.


Snijckers, R.P.M. and A.C. Foks, Adaptive immunity and atherosclerosis: aging at its crossroads. Frontiers in Immunology, 2024. 15.




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