A new role for interleukin-7 in the induction of LFA-1 and VLA-4 adhesion molecules in Phorbol 12myristate 13acetate activated CD4+ CD23+ T-cell subset.

BACKGROUND

The low affinity receptor for IgE, CD23, has been described in several pathological conditions. However, the factors involved in the upregulation or downregulation of this receptor are still debated.

METHODS AND RESULTS

We studied the effect of interleukin 7 (IL-7) on the expression of CD23 in normal PBT cells stimulated with PMA + Ca2. The data indicate that activated PB-T cultured in the presence of IL-7 showed an increased expression of CD23. The induction of IL-7 on CD23 production appears to be independent of IL-2, IL-4, IL-9, IL-15. Indeed, the addition of specific MoAbs anti-IL-2, IL-4, IL-9, IL-15 or anti-IL2R was unable to block the effect of IL-7 on CD23. The addition of IL-7 to a specific subset CD4+ CD23+ was able to augment the adhesiveness of T cells to parenchymal cell monalayers. The use of different cytokine (IL-2, IL-4, IL-9, IL-15) resulted in no increase of adhesiveness. In contrast the addition of IL-7 to a different T-cell subset (i.e. CD4+ CD23-) was unable to rescue the lack of adhesiveness observed in these cells. Blocking experiments with MHM6 MoAb were able to drastically reduce the adhesiveness observed in CD4+ CD23+ subsets. The presence of LFA-1 and VLA-4 adhesion molecules were responsible for the augmented adhesiveness of activated CD4+ CD23+ T cells cultured in the presence of IL-7. Blocking experiments with anti-LFA-1, VLA-4, anti-LFA-1beta plus VLA-4alpha MoAbs or anti-ICAM-1 MoAb added to the monolayers resulted in a complete inhibition of adhesion to parenchymal monolayers. In contrast, the addition of anti-IL-7 or anti-IL-7R MoAbs were able to block the augmented adhesiveness of CD4+ CD23+ cells to monolayers observed in the presence of IL-7.

CONCLUSION

Taken together these findings point to the likelihood that IL-7 is responsible for the observed quantitative difference in the level of adhesion molecules and may open a new role of CD23 in the immune regulation.