Activated T lymphocytes bind in situ to stromal tissue of colon carcinoma but lack adhesion to tumor cells

It is not entirely clear which adhesion molecules are responsible for the s ite-directed traffic of T cells within the tumor microenvironment. The pres ent study investigated whether colon carcinoma tissue and normal colon diff er in the expression of functionally relevant molecules. In addition, we id entified adhesion molecules involved in the binding of activated T cells on to colon carcinoma in situ. Malignant colon epithelium expressed few adhesi on receptors, i.e. CD44 (HERMES), CD49b (integrin a2) and CD162 (PSGL-1), w hereas the stromal compartment within colon carcinoma was positive for nume rous binding molecules, e.g. CD44, CD49a (integrin all, CD49e (integrin alp ha5), CD51 (integrin alpha (v)), CD54 (ICAM-1), CD99 (MIC2) and CD162. Lymp hocytes infiltrating tumor stroma contrasted with lymphocytes within normal colon interstitium by lacking CD28, CD154 (CD40L), CD56 (NCAM) and CD98 (4 F2). Normal activated T cells bound to the lymphocyte-rich areas within the stroma of colon carcinoma using CD44, CD50 (ICAM-3), CD99, CD102 (ICAM-2) and CD162 on the T lymphocytes. We conclude that lymphocytes within colon c arcinoma stroma may lack several functionally crucial cell surface molecule s. We present a panel of adhesion molecules that could mediate the migratio n of activated T lymphocytes into the stroma of colon carcinoma.