IMMUNOLOGY OF THE LUNG IN HIV-INFECTED INDIVIDUALS

The variety and frequency of pulmonary infections encountered in HIV- infected individuals indicates that many components of the host defense network are impaired. In addition to depletion of CD4+ lymphocytes, HIV results in functional deficits in CD4+ lymphocytes, CD8+ lymphocytes, and natural killer cells. Although some components of macrophage defense are preserved, lack of activation signals from CD4+ lymphocytes contributes to impaired defense by macrophages. There are few data examining the functional capabilities of neutrophils in the lung, but evidence from peripheral blood neutrophils indicates that defense by these cells is also impaired. Although the CD4+ lymphocyte is the central actor in host defense against P. carinii, impaired functions of CD8+ lymphocytes, B lymphocytes, macrophages, and neutrophils also contribute. Susceptibility to tuberculosis, another common cause of pulmonary infection in HIV-infected individuals, depends upon impaired function of both T lymphocytes and macrophages. Bacterial pneumonias are increasing in frequency in HIV-infected individuals, and impaired host defenses of the upper and lower respiratory tract are responsible. Because of the complex nature of host defenses, it is unlikely that single therapeutic maneuvers can restore functionality of all aspects of defense. However, an improved understanding of these events in the lung can lead to specific interventions aimed at restoration of deficient function.