Y. Oishi et al., CD4(-)CD8(-) T cells bearing invariant V alpha 24J alpha Q TCR alpha-chainare decreased in patients with atopic diseases, CLIN EXP IM, 119(3), 2000, pp. 404-411
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.