CD4(-)CD8(-) T cells bearing invariant V alpha 24J alpha Q TCR alpha-chainare decreased in patients with atopic diseases

Atopic disorders are caused by disregulated activation of T helper 2 (Th2) cells that produce IL-4 and IL-5. Because the presence of IL-4 potently aug ments the differentiation of naive T cells into Th2 cells, it is important to seek the cell population which provides IL-4 for naive T cells. Recently , a unique subpopulation of T cells, natural killer (NK) T cells, has been shown to produce a large amount of IL-4 upon activation, suggesting their r egulatory role in initiation of Th2 cell differentiation. To determine whet her NK T cells play a regulatory role in human Th2 cell-mediated atopic dis eases, we analysed the frequency of invariant V alpha 24J alpha Q CD4(-)CD8 (-) double-negative (DN) T cells, human NK T cells, in patients with atopic asthma and atopic dermatitis. We also studied cytokine production from V a lpha 24(+) V beta 11(+) DN T cells, which comprise most of V alpha 24J alph a Q DN T cells. We found that the invariant V alpha 24J alpha Q DN T cells were greatly diminished in patients with asthma and atopic dermatitis. On t he other hand, there was no significant difference in V alpha 24(+) CD4(+) T cells possessing invariant V alpha 24J alpha Q TCR between healthy subjec ts and atopic patients. We also found that V alpha 24(+) V beta 11(+) DN T cells from healthy subjects predominantly produced interferon-gamma (IFN-ga mma) but not IL-4 upon activation. These results suggest that NK T cells ma y not be essential for human atopic disease and that the disappearance of N K T cells, most of which produce IFN-gamma, may be involved in the pathogen esis of atopic diseases.