| Literature DB >> 25232180 |
Pia Kvistborg1, Daisy Philips2, Sander Kelderman2, Lois Hageman2, Christian Ottensmeier3, Deborah Joseph-Pietras3, Marij J P Welters4, Sjoerd van der Burg4, Ellen Kapiteijn4, Olivier Michielin5, Emanuela Romano5, Carsten Linnemann2, Daniel Speiser5, Christian Blank2, John B Haanen2, Ton N Schumacher1.
Abstract
Anti-CTLA-4 treatment improves the survival of patients with advanced-stage melanoma. However, although the anti-CTLA-4 antibody ipilimumab is now an approved treatment for patients with metastatic disease, it remains unknown by which mechanism it boosts tumor-specific T cell activity. In particular, it is unclear whether treatment amplifies previously induced T cell responses or whether it induces new tumor-specific T cell reactivities. Using a combination ultraviolet (UV)-induced peptide exchange and peptide-major histocompatibility complex (pMHC) combinatorial coding, we monitored immune reactivity against a panel of 145 melanoma-associated epitopes in a cohort of patients receiving anti-CTLA-4 treatment. Comparison of pre- and posttreatment T cell reactivities in peripheral blood mononuclear cell samples of 40 melanoma patients demonstrated that anti-CTLA-4 treatment induces a significant increase in the number of detectable melanoma-specific CD8 T cell responses (P = 0.0009). In striking contrast, the magnitude of both virus-specific and melanoma-specific T cell responses that were already detected before start of therapy remained unaltered by treatment (P = 0.74). The observation that anti-CTLA-4 treatment induces a significant number of newly detected T cell responses-but only infrequently boosts preexisting immune responses-provides strong evidence for anti-CTLA-4 therapy-enhanced T cell priming as a component of the clinical mode of action.Entities:
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Year: 2014 PMID: 25232180 DOI: 10.1126/scitranslmed.3008918
Source DB: PubMed Journal: Sci Transl Med ISSN: 1946-6234 Impact factor: 17.956