We assessed the role of the nonclassical class I molecule, CD1d, in th
e interaction between intestinal epithelial cells and T cells. In a mi
xed lymphocyte reaction (MLR) system where the stimulator cells were i
rradiated normal intestinal cells, the anti-CD1d monoclonal antibody (
mAb) 3C11 inhibited T cell proliferation. In contrast, no inhibition w
as seen when mAb 3C11 was added to conventional MLR cultures (non T ce
ll stimulators). Furthermore, no inhibition was seen when either airwa
y epithelial cells were used as stimulator cells or lamina propria lym
phocytes were used as responder cells. These latter two conditions alo
ng with a conventional MLR favor CD4+ T cell proliferation. However, w
e have previously shown that normal intestinal epithelial cells stimul
ate CD8+ T cells under similar culture conditions. Thus, CD1d expresse
d on intestinal epithelial cells may be an important ligand in CD8+ T
cell-epithelial cell interactions.