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Antigen-specific immune response and characterization of polyclonal and PSA-specific T cells in prostate cancer

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  1. Tez No: 402523
  2. Yazar: MUAMMER ALPER KURŞUNEL
  3. Danışmanlar: PROF. DR. ANDREAS THIEL, DR. NINA BABEL
  4. Tez Türü: Yüksek Lisans
  5. Konular: Üroloji, Urology
  6. Anahtar Kelimeler: Belirtilmemiş.
  7. Yıl: 2013
  8. Dil: İngilizce
  9. Üniversite: Charité–Universitätsmedizin Berlin
  10. Enstitü: Yurtdışı Enstitü
  11. Ana Bilim Dalı: Belirtilmemiş.
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: 67

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Özet (Çeviri)

Prostate cancer has the highest ratio of new cancer cases among the male population and requires additional therapeutic strategies due to its relapse and metastasis rate. Expression of tumor-associated antigens such as PSA (prostate-specific antigen) creates the opportunity to develop immunotherapy strategies for prostate cancer. However, the differences between prostate cancer patients and healthy individuals concerning the PSA-specific immune response frequencies, phenotypes and functional state of polyclonal and PSA-specific CD8+ T cells are poorly understood. In this study, PBMCs (peripheral blood mononuclear cells) from both patients and healthy donors were stimulated with PSA peptide pool and PSA-specific T cell responses in both groups were determined. Furthermore, the phenotypic differences of polyclonal and PSA-specific CD8+ T cells between prostate cancer patients and healthy donors were analyzed. In addition, tested a novel prostate cancer biomarker, zona pellucida 3 (ZP3), was tested to detect ZP3-specific T cells in prostate cancer patients. Our data showed that prostate cancer patients have significantly decreased chance to react to PSA in comparison to healthy donors. The ability of PSA-specific T cell response was limited with CD8+ T cells and could not be correlated with the stage of the disease or the quantity of PSA(146-154)-specific CD8+ T cell number. Elevated activated CD38+CD8+ T cell frequencies were observed in both polyclonal and PSA(146-154)-specific CD8+ cells in prostate cancer patients compared to the healthy donors. However, activated CD38+CD8+ T cells mainly express TIM3 (T-cell immunoglobulin domain and mucin domain 3) thus show an exhausted phenotype in prostate cancer patients. Considerably higher TIM3 expressing CD8+ T cell frequencies were also found in non-responsive patients compared to the responsive patients. Therefore, we concluded that exhaustion of CD8+ T cells in prostate cancer patients might be a major factor in the lack of response to PSA in comparison to healthy donors. Additionally, higher CCR4 (C-C chemokine receptor type 4 )/ CCR5 (C-C chemokine receptor type 5) ratio on CD8+ T cells was found in prostate cancer patients than healthy individuals. CCR4 is associated with type-2 response thus is proposed to promote tumor progression. Imbalance between chemokine receptors towards CCR4 and it is possible attraction by the tumor might also interfere cytotoxic CD8+ T cell response in prostate cancer patients.

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