TRANSFORMING GROWTH FACTOR-BETA(1)-INDUCED EXPRESSION OF THE MUCOSA-RELATED INTEGRIN ALPHA(E) ON LYMPHOCYTES IS NOT ASSOCIATED WITH MUCOSE-SPECIFIC HOMING

The integrin alpha(E) (HML-1, alpha(IEL), alpha(M290)) is largely expressed on lymphocytes in epithelial sites, especially the gut mucosa. We investigated whether alpha(E) has any role in homing or delineates a phenotype with distinct migratory behavior. Lymph node T cells were stimulated for 5 days with anti-CD3 in the presence or absence of transforming growth factor (TGF)beta(1), to generate alpha(E)(+) or alpha(E)(-) cells, respectively. The two populations were then tested for their homing properties in mice. Both alpha(E)(+) (TGF-beta-treated) and alpha(E)(-) (control) cells of either CD4(+) or CD8(+) subset had a low capacity to enter the gut and showed the same homing behavior with respect to a variety of other organs. The same was true for alpha(E)(+) and alpha(E)(-) cells that had been briefly stimulated with anti-CD3 (24 h) and then allowed to return to a resting state before injection, though in this case both populations showed a greater capacity to recirculate through lymphoid tissue than was seen with fully activated eels. The results indicate that alpha(E) beta(7) does not act as a homing receptor, and that the expression of the site-specific marker alpha(E) does not correlate with a distinct homing behavior.