Cellular and Molecular Life Sciences

, Volume 69, Issue 10, pp 1615–1623

Immune aging and autoimmunity

Multi-author review

DOI: 10.1007/s00018-012-0970-0

Cite this article as:
Goronzy, J.J. & Weyand, C.M. Cell. Mol. Life Sci. (2012) 69: 1615. doi:10.1007/s00018-012-0970-0


Age is an important risk for autoimmunity, and many autoimmune diseases preferentially occur in the second half of adulthood when immune competence has declined and thymic T cell generation has ceased. Many tolerance checkpoints have to fail for an autoimmune disease to develop, and several of those are susceptible to the immune aging process. Homeostatic T cell proliferation which is mainly responsible for T cell replenishment during adulthood can lead to the selection of T cells with increased affinity to self- or neoantigens and enhanced growth and survival properties. These cells can acquire a memory-like phenotype, in particular under lymphopenic conditions. Accumulation of end-differentiated effector T cells, either specific for self-antigen or for latent viruses, have a low activation threshold due to the expression of signaling and regulatory molecules and generate an inflammatory environment with their ability to be cytotoxic and to produce excessive amounts of cytokines and thereby inducing or amplifying autoimmune responses.


AgeAutoimmunityT cell memoryT cell homeostasisCD45RA T effector cells



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Copyright information

© Springer Basel AG (outside the USA) 2012

Authors and Affiliations

  1. 1.Division of Immunology and Rheumatology, Department of MedicineStanford University School of MedicineStanfordUSA