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

Effector functions of CD4-CD8- double negative (DN) alpha beta TCR+ cellswere examined. Among mouse DN alpha beta TCR+ thymocytes, NK1.1+ cellsexpressing a canonical V alpha 14/J alpha 281 TCR but not NK1.1- cellsproduce IL-4 upon TCR cross-linking and IFN-gamma upon cross- linking ofNK1.1 as well as TCR. Production of IL-4 but not IFN-gamma from DN alphabeta TCR+NK1.1+ cells was markedly suppressed by IL-2. Whereas V alpha 14/Jalpha 281 TCR+ cells express NK1.1+, these cells are not the precursor ofDN alpha beta TCR+NK1.1+CD16+B220+ large granular lymphocytes (LGL). IL-2induces rapid proliferation and generation of NK1.1+ LGL from DN alpha betaTCR+NK1.1- but not from DN alpha beta TCR+NK1.1+ cells. LGL cells exhibitNK activity and produce IFN-gamma but not IL-4 upon cross-linking ofsurface TCR or NK1.1 molecules. In contrast to IL-2, IL-7 does not induceLGL cells or NK activity from DN alpha beta TCR+NK1.1- cells but inducesthe ability to produce high levels of IL-4 upon TCR cross-linking. Ourresults show that DN alpha beta TCR+ T cells have several distinctsubpopulations, and that IL-2 and IL-7 differentially regulate thefunctions of DN alpha beta TCR+ T cells by inducing different types ofeffector cells.