T-cell homeostasis appears to be maintained throughout much of normal adult life independent of de-novo production from hematopoietic stem cells via thymopoiesis. Instead, peripheral mechanisms are generally sufficient to maintain normal T-cell number, function and adequate TCR repertoire diversity in healthy hosts. Studies of T-cell regeneration in animals, however, have shown that full restoration of T-cell homeostasis after profound T-cell depletion is primarily dependent upon thymopoiesis. In this setting, thymic-deficient hosts have prolonged reductions in total T-cell number, restricted TCR repertoire diversity, and limited immunocompetence. In humans, age-related reductions in thymic regenerative capacity as early as young adulthood result in incomplete restoration of T-cell homeostasis after T-cell depletion.
Copyright 1997 United States Government.