Human intraepithelial lymphocytes (IEL), predominantly CD8+ T-lymphocytes located between intestinal epithelial cells (EC), may represent the first-line immune defense against colon cancer. The mechanism by which IEL bind to the colon cancer line, DLD-1, was evaluated.

A larger fraction of IEL than peripheral blood mononuclear cells bound to DLD-1 monolayers (25 ± 16 versus 8 ± 4% binding, P < 0.05). Binding increased when DLD-1 monolayers were incubated with interferon-γ but not with tumor necrosis factor-α. Similar numbers of IEL adhered to EC tumors, HT-29 and 5637, and the non-EC tumor, A375, but fewer bound to nonmalignant smooth muscle (HISM) and fibroblast (KD) lines (P < 0.01). Binding of IEL to DLD-1 was reduced by monoclonal antibodies to HML-1 and CD11a (47 ± 9 and 26 ± 13% inhibition, respectively) and was completely eliminated by both combined (93 ± 4% inhibition). Anti-HML-1 also inhibited the binding of IEL to other EC tumors but did not affect binding to non-EC tumors or fibroblasts. To conclude, the binding of IEL to EC tumors is mediated by HML-1 and CD11a [A. I. Roberts, S. M. O'Connell, and E. C. Ebert. Binding of intraepithelial lymphocytes to colon cancer cells is mediated by HML-1 and LFA-1 (abstract). Gastroenterology, 102: A685, 1992].


This project was funded by a grant from the NIH (DK 42166).

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