Age-associated alterations of the immune response (immunosenescence) have a strong clinical impact and contribute to autoimmune morbidity (frailty) and mortality in the elderly. Immunosenescence is characterized by i) thymic involution leading to a steady decline in the production of naïve T cells, ii) shrinkage of the T cell repertoire through continuous antigen stimulation favoring the development of functionally altered, oligoclonal, senescent T cells (identified by CD28 loss and telomere shortening) and iii) a chronic low degree of inflammation (termed inflamm-aging) as evidenced by increased serum levels of inflammatory cytokines and acute phase proteins.
It is currently not known how aging affects the prevalence and functionality of different immune cell subsets. The altered cytokine milieu as a consequence of inflamm-aging may 1/ accelerate replicative senescence in T cells and 2/ favour a shift (away) from the Treg effector arm of the immune system towards the pro-inflammatory Th17 effector subset associated with tissue pathology. Both processes may contribute to the decline in peripheral T cell numbers and the development of an immune risk phenotype. In addition, other immune cell subsets, such as antigen presenting cells and NK/T cells, may be affected and involved in the process of immunosenescence.
|Last modified:||16 June 2015 2.04 p.m.|