American Journal of Immunology

Foxp3-Mediated Immunity of Human Pancreatic Cancer Cell Line PANC-1

Renxi Wang, Gencheng Han, Jianan Wang, Guojiang Chen, Ruonan Xu, Liyan Wang, Xia Li, Beifen Shen and Yan Li

DOI : 10.3844/ajisp.2009.101.107

American Journal of Immunology

Volume 5, 2009

Pages 101-107

Abstract

Problem statement: More and more evidences have shown that human cancer cells can express Foxp3, the regulatory T cell-associated transcription factor. The role of Foxp3 in human cancer cells is still unclear. We detected Foxp3 expression in human pancreatic cancer cell line PANC-1. SiRNA assays showed that Foxp3 expression suppressed the expression of TGF-β and IL-10 which could induce immune tolerance. Approach: Thus, we proposed that Foxp3 expression in PANC-1 cells controlled the response but not tolerance characteristics of the cells. To prove the proposal, we first developed the PANC-1 cell-induced the immune response model. PANC-1 cells induced response in autoimmune Non-Obese Diabetes (NOD) mice aged of >12 weeks. In vitro cell co-cultured assay demonstrated that PANC-1 induced response in splenocytes from NOD mice aged of >12 weeks. Results: In the same time, we found that inflammatory cytokine such as INF-γ, IL-2 and IL-17 increased and anti-inflammatory cytokine such as IL-4, IL-10 and TGF-β decreased in the co-cultured supernatant. These results demonstrate that PANC-1 cells induced response in splenocytes from NOD mice aged of >12 weeks. SiRNA assays showed that Foxp3 in PANC-1 cells controlled the response in the co-cultured cells. Conclusion: The results suggested that Foxp3 control the immunological response characteristics of PANC-1 cells in autoimmune condition.

Copyright

© 2009 Renxi Wang, Gencheng Han, Jianan Wang, Guojiang Chen, Ruonan Xu, Liyan Wang, Xia Li, Beifen Shen and Yan Li. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.