Ba. Spain et al., ENHANCED PROLIFERATION AND IL-2 SECRETION BY LUNG LYMPHOCYTES FROM HIV-INFECTED SUBJECTS, American journal of physiology. Lung cellular and molecular physiology, 13(4), 1995, pp. 498-506
Human immunodeficiency virus (HIV)-positive patients frequently develo
p a CD3(+)/CD8(+) cytotoxic T cell lymphocytic alveolitis. This could
occur through in situ expansion of lung lymphocytes. We evaluated lung
and blood lymphocyte proliferation in asymptomatic HIV-infected indiv
iduals by measuring spontaneous and cytokine-induced tritiated thymidi
ne incorporation. Interleukin (IL)-2 and IL-4 secretion was determined
with the use of enzyme-linked immunosorbent assay. Western blotting,
and immunoprecipitation techniques. Spontaneous proliferation by lung
lymphocytes from HIV-positive patients was significantly greater than
that of normal volunteers. Proliferation was confined to the CD8(+) ly
mphocyte subset. Over time, spontaneous proliferation declined unless
autologous alveolar macrophages (AM) were added, suggesting AM were pr
oviding additional stimulatory signals to lung lymphocytes. Lung and b
lood lymphocytes proliferated in response to IL-2 but not IL-4. Lympho
cytes in HIV-infected lung spontaneously produced and secreted more IL
-2 than either normal lung lymphocytes or autologous blood lymphocytes
. IL-4 production was not detectable in either group. These findings s
upport the hypothesis that lymphocytic alveolitis in asymptomatic HIV-
positive patients results from IL-2-dependent in situ proliferation of
CD3(+)/CD8(+) cytotoxic T cells.