Browse by author
Lookup NU author(s): Joanne Cresswell, Matthew Henry, Dr Helen Robertson, Professor David Neal, Emeritus Professor John Kirby
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
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.
Author(s): Henry MJ; Kirby JA; Cresswell J; Neal DE; Robertson H; Wong W
Publication type: Article
Publication status: Published
Journal: Cancer Immunology, Immunotherapy
Year: 2002
Volume: 51
Issue: 9
Pages: 483-491
ISSN (print): 0340-7004
ISSN (electronic): 1432-0851
Publisher: Springer
URL: http://dx.doi.org/10.1007/s00262-002-0305-3
DOI: 10.1007/s00262-002-0305-3
PubMed id: 12357319
Altmetrics provided by Altmetric