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- Title
Adhesion of lymphocytes to bladder cancer cells: the role of the α<sub>E</sub>β<sub>7</sub> integrin.
- Authors
Cresswell, Joanne; Wong, Wai Keong; Henry, Matthew J.; Robertson, Helen; Neal, David E.; Kirby, John A.
- Abstract
The αEβ7 integrin (defined by CD103) is expressed by most intra-epithelial lymphocytes (IEL) but by fewer than 2% peripheral blood lymphocytes (PBL). An important ligand for this molecule is the epithelial cell adhesion molecule E-cadherin. Loss of E-cadherin is associated with increased invasion and metastasis in bladder cancer. This study examines the role of the αEβ7–E-cadherin interaction in lymphocyte targeting of bladder cancer cells. Lymphocytes were activated in vitro by mixed lymphocyte reaction (MLR) and CD103 was upregulated by treatment with transforming growth factor β (TGFβ). The CD103+ lymphocytes were used in a flow cytometric adhesion assay with bladder cancer cell lines, differing in expression of E-cadherin and intercellular adhesion molecule-1 (ICAM-1). Antibody blockade was used to confirm the relative importance of CD103 and ICAM-1 to intercellular adhesion. Lymphocytes with upregulated CD103 compared to control lymphocytes showed enhanced adhesion to an E-cadherin expressing bladder cancer cell line (P=0.0003). This increased adhesion could be abrogated by anti-CD103 adhesion blockade. For ICAM-1 expressing bladder cells, adhesion of lymphocytes could be markedly reduced using anti-ICAM-1 blockade. In conclusion, the upregulation of CD103 by lymphocytes increases adhesion to E-cadherin expressing bladder cancer targets. Loss of E-cadherin in bladder cancer progression may provide a mechanism both for increased invasion and effective immune evasion.
- Subjects
CELL adhesion molecules; INTEGRINS; GLYCOPROTEINS; PLATELET glycoprotein GPIIb-IIIa complex; BIOMOLECULES; LYMPHOCYTES; CANCER cells; TUMOR immunology
- Publication
Cancer Immunology, Immunotherapy, 2002, Vol 51, Issue 9, p483
- ISSN
0340-7004
- Publication type
Article
- DOI
10.1007/s00262-002-0305-3