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Ebelt, K. ; Babaryka, G.* ; Frankenberger, B. ; Stief, C.G.* ; Eisenmenger, W.* ; Kirchner, T.* ; Schendel, D.J. ; Nößner, E.

Prostate cancer lesions are surrounded by FOXP3⁺, PD-1⁺ and B7-H1⁺ lymphocyte clusters.

Eur. J. Cancer 45, 1664-1672 (2009)
Open Access Green as soon as Postprint is submitted to ZB.
The immune response against prostate cancer seems to be inefficient although tumour cells show an over-expression of tumour-associated antigens suggesting that regulatory networks inhibit immune cell function locally. To address this proposition, lymphocytes within prostate cancer-inflicted tissue were analysed for the expression of markers associated with negative regulatory function and exhaustion. Prostate cancer, benign prostatic hyperplasia and healthy prostate tissues were investigated by immunohistology for CD25, FOXP3, PD-1 and B7-H1. We had previously documented that prostate cancer islets are surrounded by clustered accumulations of CD3(+) lymphocytes, which lack perforin and interferon-gamma (IFN gamma) expression, thus are apparently quiescent. Here, we report that these clusters contain numerous CD25(+) and FOXP3(+) cells. These markers are associated with regulatory T cells, and their presence in lymphocyte clusters near prostate cancer regions indicates an environment with negative impact on immune response against cancer cells. Consistent with this hypothesis, cells expressing PD-1 and its ligand B7-H1, which are markers associated with exhaustion of lymphocyte function, were also detected in the lymphocyte clusters. Expression of molecules associated with inhibition and exhaustion of lymphocytes may reflect events contributing to ineffective immune responses against cancer cells.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Tumour-infiltrating lymphocytes; FOXP3; Tregs; PD-1; B7-H1; Exhausted lymphocytes; regulatory t-cells; infiltrating lymphocytes; carcinoma patients; expression; immunology; prognosis; diseases; target
ISSN (print) / ISBN 0959-8049
e-ISSN 1879-0852
Quellenangaben Volume: 45, Issue: 9, Pages: 1664-1672 Article Number: , Supplement: ,
Publisher Elsevier
Reviewing status Peer reviewed