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Παρασκευή 7 Δεκεμβρίου 2018

Immunosuppressive {beta}ig-h3 links tumour stroma and dysfunctional T cells in pancreatic cancer

Recent FDA approval of anti-PD-1 antibody pembrolizumab as a site-agnostic therapy for mismatch repair (MMR)–deficient solid tumours has highlighted the importance of CD8+ T cell responses and the potential of immunotherapy, even in tumour entities that are traditionally considered poor candidates for immune-based therapies, such as pancreatic carcinoma.1 Clearly, the old dogma of immunologically cold pancreatic carcinoma has to be refined.

It has been known for long that higher levels of intratumoural CD8+ cytotoxic T lymphocytes (CTLs) correlate with better survival of patients with pancreatic carcinoma.2 3 However, in most pancreatic carcinomas, endogenous CD8+ T cells are relatively sparse.4 Moreover, intratumoural macrophages, myeloid-derived suppressor cells and regulatory T cells (Tregs) dominate even the earliest phases of pancreatic cancer development, and predominance of these immunosuppressive cell populations persists through invasive cancer. This immune privilege of pancreatic cancer is characterised by a comparatively low mutational burden resulting in fewer...



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