Immunosenescence, the progressive decline in immune function that develops with age, results from cumulative alterations in critical B- and T-cell subpopulations. Decreases in circulating memory B cells and in germinal center formation are evident in the elderly, possibly due to diminished follicular dendritic-cell function. T-cell dysfunction is associated with reduced thymic generation of naïve T cells, virus-induced expansion of terminal effectors and increased levels of memory cells producing type I and II cytokines. The diversity of the T-cell receptor repertoire is diminished by the first two changes, and elevated type I cytokines might contribute to the pro-inflammatory cytokine milieu present in the elderly.