A novel role for polymeric immunoglobulin receptor in tumour development: beyond mucosal immunity and into hepatic cancer cell transformation

Dewdney, Brittany Alexandra, and Hebbard, Lionel (2018) A novel role for polymeric immunoglobulin receptor in tumour development: beyond mucosal immunity and into hepatic cancer cell transformation. HepatoBiliary Surgery and Nutrition, 7 (1). pp. 52-55.

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Chronic inflammation is well known as a significant driver of carcinogenesis in settings of human disease, including liver disease and hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) is one of the major causes of HCC due to the oncogenic nature of the virus and the robust inflammatory response in the infected host. Fc receptors (FcR) are specialized receptors found on innate immune cells that recognize and bind to antigen-presenting antibodies, linking the innate and adaptive immune system to respond to circulating foreign bodies, such as viral DNA (1). Increased B-cell activation and antibody production in response to HBV infected liver will lead to increased FcR signalling on circulating innate immune cells and resident-macrophages (Kupffer cells), further enhancing the inflammatory response. Progression to chronic liver inflammation is associated with hyperactivity of B cell immunity, increasing the risk of cancer development due to constant infiltration of immune cells and accumulation of damaged hepatocytes. FcR activation has been previously implicated in carcinogenesis by creating a ‘pro-tumour microenvironment’ within inflammation-mediated damaged tissue through promotion of angiogenesis, epithelial mesenchymal transition (EMT), and increased cell survival (2). Of recent interest is the polymeric immunoglobulin receptor (pIgR), a member of the Fc receptor family, that is widely expressed on epithelial cells and is responsible for transcytosis of IgA/IgM at mucosal surfaces. Few studies have investigated the role of pIgR in cancer, although most have implicated pIgR to be downregulated in cancers of various epithelial origin (3). In this sense, the dysregulation of pIgR in mucosal membranes could limit the first line of defence for immunity against carcinogenic cells, and possibly contribute to malignant transformation.

Item ID: 53973
Item Type: Article (Editorial)
ISSN: 2304-389X
Copyright Information: Copyright © HepatoBiliary Surgery and Nutrition. All rights reserved. Open Access Policy This journal provides immediate open access to its content on the principle that making research freely available to the public supports a greater global exchange of knowledge.
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Hepatobiliary Surg Nutr; HBSN) is an open access, peer-reviewed, bi-monthly journal (Dec. 2012-).

Funders: Cancer Council NSW (CC), James Cook University (JCU), Cancer Council Queensland (CCQ)
Projects and Grants: CC grant 1069733, CQU grant 1123436, James Cook Development Grant 2016, JCU Postgraduate Research Stipend Scholarship
Date Deposited: 31 Oct 2018 03:01
FoR Codes: 11 MEDICAL AND HEALTH SCIENCES > 1112 Oncology and Carcinogenesis > 111201 Cancer Cell Biology @ 100%
SEO Codes: 92 HEALTH > 9201 Clinical Health (Organs, Diseases and Abnormal Conditions) > 920102 Cancer and Related Disorders @ 100%
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