TY - JOUR
AU - Meng, Zibo
AU - Rodriguez Ehrenfried, Aaron
AU - Tan, Chin Leng
AU - Steffens, Laura Katharina
AU - Kehm, Hannes
AU - Zens, Stefan
AU - Lauenstein, Claudia
AU - Paul, Alina
AU - Schwab, Marius
AU - Förster, Jonas
AU - Salek, Mogjiborahman
AU - Riemer, Angelika
AU - Wu, Heshui
AU - Eckert, Christoph
AU - Leonhardt, Carl-Stephan
AU - Strobel, Oliver
AU - Volkmar, Michael
AU - Poschke, Isabel
AU - Offringa, Rienk
TI - Transcriptome-based identification of tumor-reactive and bystander CD8+ T cell receptor clonotypes in human pancreatic cancer.
JO - Science translational medicine
VL - 15
IS - 722
SN - 1946-6234
CY - Washington, DC
PB - AAAS
M1 - DKFZ-2023-02366
SP - eadh9562
PY - 2023
N1 - #EA:D200#EA:D170#LA:D200#LA:D170# / HI-TRON
AB - Pancreatic ductal adenocarcinoma (PDAC) is generally refractory to immune checkpoint blockade, although patients with genetically unstable tumors can show modest therapeutic benefit. We previously demonstrated the presence of tumor-reactive CD8+ T cells in PDAC samples. Here, we charted the tumor-infiltrating T cell repertoire in PDAC by combining single-cell transcriptomics with functional testing of T cell receptors (TCRs) for reactivity against autologous tumor cells. On the basis of a comprehensive dataset including 93 tumor-reactive and 65 bystander TCR clonotypes, we delineated a gene signature that effectively distinguishes between these T cell subsets in PDAC, as well as in other tumor indications. This revealed a high frequency of tumor-reactive TCR clonotypes in three genetically unstable samples. In contrast, the T cell repertoire in six genetically stable PDAC tumors was largely dominated by bystander T cells. Nevertheless, multiple tumor-reactive TCRs were successfully identified in each of these samples, thereby providing a perspective for personalized immunotherapy in this treatment-resistant indication.
LB - PUB:(DE-HGF)16
C6 - pmid:37967201
DO - DOI:10.1126/scitranslmed.adh9562
UR - https://inrepo02.dkfz.de/record/285421
ER -