Delvecchio FR, Goulart MR, Fincham REA, Bombadieri M, Kocher HM. B cells in pancreatic cancer stroma. World J Gastroenterol 2022; 28(11): 1088-1101 [PMID: 35431504 DOI: 10.3748/wjg.v28.i11.1088]
Corresponding Author of This Article
Hemant M Kocher, FRCS (Gen Surg), MBBS, MD, MS, Professor, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, London, United Kingdom. h.kocher@qmul.ac.uk
Research Domain of This Article
Oncology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Mar 21, 2022; 28(11): 1088-1101 Published online Mar 21, 2022. doi: 10.3748/wjg.v28.i11.1088
B cells in pancreatic cancer stroma
Francesca Romana Delvecchio, Michelle R Goulart, Rachel Elizabeth Ann Fincham, Michele Bombadieri, Hemant M Kocher
Francesca Romana Delvecchio, Michele Bombadieri, William Harvey Research Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom
Francesca Romana Delvecchio, Michelle R Goulart, Rachel Elizabeth Ann Fincham, Hemant M Kocher, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom
Hemant M Kocher, Barts and the London HPB Centre, Barts Health NHS Trust, London E1 1BB, United Kingdom
Author contributions: Delvecchio FR review the literature, Delvecchio FR and Kocher HM drafted the original manuscript; Delvecchio FR composed the original figures; Delvecchio FR, Goulart MR, Fincham REA, Bombardieri M and Kocher HM contributed to the review and editing of the manuscript.
Supported byFrancesca Romana Delvecchio is supported by Cancer Research UK Post-doctoral fellowship; Michelle Goulart is supported by PCRF post-doctoral fellowship; Rachel Elizabeth Ann Fincham is supported by PhD studentship awarded by Barts Charity (London, UK) and A*STAR (Singapore).
Conflict-of-interest statement: There are no conflicts of interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hemant M Kocher, FRCS (Gen Surg), MBBS, MD, MS, Professor, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, London, United Kingdom. h.kocher@qmul.ac.uk
Received: April 9, 2021 Peer-review started: April 9, 2021 Revised: May 18, 2021 Accepted: February 19, 2022 Article in press: February 19, 2022 Published online: March 21, 2022 Processing time: 341 Days and 7 Hours
Abstract
Pancreatic cancer is a disease with high unmet clinical need. Pancreatic cancer is also characterised by an intense fibrotic stroma, which harbours many immune cells. Studies in both human and animal models have demonstrated that the immune system plays a crucial role in modulating tumour onset and progression. In human pancreatic ductal adenocarcinoma, high B-cell infiltration correlates with better patient survival. Hence, B cells have received recent interest in pancreatic cancer as potential therapeutic targets. However, the data on the role of B cells in murine models is unclear as it is dependent on the pancreatic cancer model used to study. Nevertheless, it appears that B cells do organise along with other immune cells such as a network of follicular dendritic cells (DCs), surrounded by T cells and DCs to form tertiary lymphoid structures (TLS). TLS are increasingly recognised as sites for antigen presentation, T-cell activation, B-cell maturation and differentiation in plasma cells. In this review we dissect the role of B cells and provide directions for future studies to harness the role of B cells in treatment of human pancreatic cancer.
Core Tip: The role of B cells in pancreatic ductal adenocarcinoma tumorigenesis is controversial. Human studies show clusters of B cells, interacting with other immune cells, forming active sites of the immune response, called tertiary lymphoid structures. In vitro experiments and in vivo studies using B-cell deficient mice suggest the role of an immuno-suppressive B cell phenotype to induce tumour-progression. These discordant findings highlight the need of further studies using better murine models to recapitulate pancreatic cancer and its immune infiltrate.
