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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)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter 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 Band: 45, Heft: 9, Seiten: 1664-1672 Artikelnummer: , Supplement: ,
Verlag Elsevier
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed