Immunology of the aging lung.

The aging process is associated with multiple deficits in pulmonary immune function. Defense of the airway is impaired in the elderly by decreased mucociliary clearance, alteration in respiratory mechanics and, in some cases, concomitant illnesses that predispose to aspiration. Alveolar defenses can be divided into resident defense mechanisms, inflammatory responses, and specific immune responses. Resident defenses such as macrophage phagocytosis and chemotaxis, although largely intact, may have subtle defects under specific conditions. Inflammatory responses may also be diminished, as evidenced by decreased neutrophil-mediated killing and chemotaxis. Specific immune responses appear to be the most vulnerable to age-associated impairment. Although antigen presentation is well preserved during aging, accessory cell cytokine production may be decreased. T-lymphocyte proliferative responses are markedly decreased, as is the production of and response to intercellular mediators. Age-associated alterations in T cell subpopulations may result in imperfect T cell-B cell interactions leading to expression of abnormal immunoglobulins. These many interacting and compounding impairments may explain the increased susceptibility of the elderly to pulmonary infection and autoimmune diseases.