This study aim to quantify the dynamic number changes of CD3(+) lymph cells in a pre-malignant stage of pancreatic cancer, namely, pancreatic intraepithelial neoplasia (PanIN). The experiment was conducted using a well-established KrasG12D/Pdx1-Cre transgenic mouse model. The animal model expressed a pancreas-specific active KrasG12D gene, resulting in PanIN progression and acinar structure loss in a time dependent manner. Experiment mice were sacrificed at 5, 7, 9, and 11 months (n = 3 for each time point). The pancreas tissues were fixed and stained by a rabbit monoclonal [EPR4517] to CD3G (Abcam Cat#: ab134096, 1:500 dilution). The CD3(+) lymph cell number were quantified by Leica optical system and the CD3(+) lymph cells were manually counted (ten fields for each mouse). All experimental conducted were approved by the ethical committee. The CD3(+) lymph cell number was calculated by averaging all field in each time point (thirty fields per time point). The number was then presented as mean ± SEM. Quantitatively, the CD3(+) cell were 11.73 ± 2.83, 14.23 ± 2.07, 14.90 ± 1.99, and 29.13 ± 2.04 per field in 5, 7, 9, and 11 month-old mice. The CD3(+) cell number was not significantly different among 5, 7, and 9 month-old mice. However, the number significantly increase in the 11 month-old mice compared with the 9-month ones (P< 0.0001, unpaired t-test). We observed that CD3(+) lymph cells were predominately present in PanIN area, while almost not observable in the remaining normal acinar area. The phenomenon that CD3(+) lymph cells infiltrate in PanIN area indicates that this type of immune cells may involve in PanIN progression.
Citation Format: Xiafei Hong, Hongmei Dai, Xianze Wang, Feng Tian, Wenming Wu, Yupei Zhao. Increased CD3(+) cell infiltration during pancreatic intraepithelial neoplasia progression in KrasG12D/Pdx1-Cre transgenic mouse model [abstract]. In: Proceedings of the Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; 2016 Sept 25-28; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(11 Suppl):Abstract nr A138.