Immunosenescence is a complex remodeling of the immune system that may contribute significantly to morbidity and mortality in the elderly. Much evidence suggests an association between immune function and well-being during aging and longevity. Despite several studies on the immune system in the elderly, little is known of the biological basis of immunosenescence in humans. Undoubtedly, some diseases to which the elderly are particularly susceptible, such as infections and autoimmune and neoplastic pathologies, include dysregulation of several immune functions in their pathogenesis. On the other hand, recent studies in healthy centenarians suggest that the immunological changes observed during aging are consistent with a reshaping, rather than a generalized deterioration, of the main immune functions. The infection rate and severity increase with aging as a result of decrease in immune function with aging. The primary changes of the aged host are in the T-lymphocytes, perhaps because of the involution of the thymus. Secondary changes (environmental) may be the result of changes in diet, drug intake, physical activity, and so forth or, alternatively, the result of underlying diseases (Wick and Grubeck-Loebenstein, 1997). There is a paradoxical increase in autoimmunity, and the responsiveness to exogenous antigens and tumors are reduced and may play a proinflammatory role in the development of many pathological conditions (Weyand et al., 1998). Recurrent stress, infections, and inflammation over the life-span play a significant role in producing age-associated changes in all systems. Genetic selection for infections has been implicated in coronary heart disease (McCann et al., 1998), early onset of Parkinson’s following influenza encephalitis, and Alzheimer’s disease (Stoessl, 1999).