Infection by a virus of an individual (aged 20-30) will cause a response from the T (thymus derived) lymphocytes of which there are approximately 3 x 1011. If the individual has not met the virus before, the response will come from the naïve T cell subset (50±10% of the total T cell pool at this age) containing recent thymic emigrants produced from the thymus at approximately 108 per day. Their antigen specific receptor has a defined specificity governed by the conformation of its 2 chains (? and ?) and the repertoire of specificities is somewhere in the region of 2 x 107 to 108. A successful response leads to clonal expansion and the generation of memory T cells to the infecting agent.
Ageing is accompanied by thymic atrophy, a reduction in thymic output and a consequent reduction in the naive T cell pool. This is not accompanied by a reduction in the absolute number of T cells because of the expansion of the memory T cell subset. Successive rounds of division within this subset may be responsible for the accrual of defects and the accumulation of senescent cells. Within the thymus, age related thymic atrophy is accompanied by a decline in the production of Interleukin 7 (IL-7), a cytokine known to have an essential role in T cell development. Therapeutic intervention with IL-7 in old mice increases both the size of the thymus and its subsequent output benefiting the functional performance of the T cells in the peripheral T cell pool.