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Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Direct measurements revealed low oxygen tensions (0.5–4.5%
oxygen) in murine lymphoid organs in vivo. To test whether
adaptation to changes in oxygen tension may have an effect on
lymphocyte functions, T cell differentiation and functions at varying
oxygen tensions were studied. These studies show: 1) differentiated CTL
deliver Fas ligand- and perforin-dependent lethal hit equally well at
all redox conditions; 2) CTL development is delayed at 2.5% oxygen as
compared with 20% oxygen. Remarkably, development of CTL at 2.5%
oxygen is more sustained and the CTL much more lytic; and 3) hypoxic
exposure and TCR-mediated activation are additive in enhancing levels
of hypoxia response element-containing gene products in lymphocyte
supernatants. In contrast, hypoxia inhibited the accumulation of
nonhypoxia response element-containing gene products (e.g., IL-2 and
IFN-
) in the same cultures. This suggests that T cell activation in
hypoxic conditions in vivo may lead to different patterns of lymphokine
secretion and accumulation of cytokines (e.g., vascular endothelial
growth factor) affecting endothelial cells and vascular
permeabilization. Thus, although higher numbers of cells survive and
are activated during 20% oxygen incubation in vitro, the CTL which
develop at 2.5% oxygen are more lytic with higher levels of activation
markers. It is concluded that the ambient 20% oxygen tension (plus
2-ME) is remarkably well suited for immunologic specificity and
cytotoxicity studies, but oxygen dependence should be taken into
account during the design and interpretation of results of in vitro T
cell development assays and gene expression studies in
vivo.
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