IL-2 and IL-7 differentially induce CD4-CD8- alpha beta TCR+NK1.1+ large granular lymphocytes and IL-4-producing cells from CD4-CD8- alpha beta TCR+NK1.1- cells: implications for the regulation of Th1- and Th2- type responses |
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Authors: | Nishizawa K; Koyasu S |
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Institution: | Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. |
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Abstract: | Effector functions of CD4-CD8- double negative (DN) alpha beta TCR+ cells
were examined. Among mouse DN alpha beta TCR+ thymocytes, NK1.1+ cells
expressing a canonical V alpha 14/J alpha 281 TCR but not NK1.1- cells
produce IL-4 upon TCR cross-linking and IFN-gamma upon cross- linking of
NK1.1 as well as TCR. Production of IL-4 but not IFN-gamma from DN alpha
beta TCR+NK1.1+ cells was markedly suppressed by IL-2. Whereas V alpha 14/J
alpha 281 TCR+ cells express NK1.1+, these cells are not the precursor of
DN alpha beta TCR+NK1.1+CD16+B220+ large granular lymphocytes (LGL). IL-2
induces rapid proliferation and generation of NK1.1+ LGL from DN alpha beta
TCR+NK1.1- but not from DN alpha beta TCR+NK1.1+ cells. LGL cells exhibit
NK activity and produce IFN-gamma but not IL-4 upon cross-linking of
surface TCR or NK1.1 molecules. In contrast to IL-2, IL-7 does not induce
LGL cells or NK activity from DN alpha beta TCR+NK1.1- cells but induces
the ability to produce high levels of IL-4 upon TCR cross-linking. Our
results show that DN alpha beta TCR+ T cells have several distinct
subpopulations, and that IL-2 and IL-7 differentially regulate the
functions of DN alpha beta TCR+ T cells by inducing different types of
effector cells.
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