Transforming growth factor-beta 1-induced expression of the mucosa-related integrin alpha E on lymphocytes is not associated with mucosa-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 cells. 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.