| pubmed-article:11169447 | pubmed:abstractText | It is not entirely clear which adhesion molecules are responsible for the site-directed traffic of T cells within the tumor microenvironment. The present study investigated whether colon carcinoma tissue and normal colon differ in the expression of functionally relevant molecules. In addition, we identified adhesion molecules involved in the binding of activated T cells onto colon carcinoma in situ. Malignant colon epithelium expressed few adhesion receptors, i.e. CD44 (HERMES), CD49b (integrin alpha2) and CD162 (PSGL-1), whereas the stromal compartment within colon carcinoma was positive for numerous binding molecules, e.g. CD44, CD49a (integrin alpha1), CD49e (integrin alpha5), CD51 (integrin alpha(v)), CD54 (ICAM-1), CD99 (MIC2) and CD162. Lymphocytes infiltrating tumor stroma contrasted with lymphocytes within normal colon interstitium by lacking CD28, CD154 (CD40L), CD56 (NCAM) and CD98 (4F2). 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 carcinoma stroma may lack several functionally crucial cell surface molecules. We present a panel of adhesion molecules that could mediate the migration of activated T lymphocytes into the stroma of colon carcinoma. | lld:pubmed |
