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Opisthorchiasis-Induced Cholangiocarcinoma: How Innate Immunity May Cause Cancer.
- Source :
-
Advances in parasitology [Adv Parasitol] 2018; Vol. 101, pp. 149-176. Date of Electronic Publication: 2018 May 29. - Publication Year :
- 2018
-
Abstract
- Innate, inflammatory responses towards persistent Opisthorchis viverrini (OV) infection are likely to contribute to the development of cholangiocarcinoma (CCA), a liver cancer that is rare in the West but prevalent in Greater Mekong Subregion countries in Southeast Asia. Infection results in the infiltration of innate immune cells into the bile ducts and subsequent activation of inflammatory immune responses that fail to clear OV but instead may damage local tissues within the bile ducts. Not all patients infected with OV develop CCA, and so tumourigenesis may be dependent on multiple factors including the magnitude of the inflammatory response that is activated in infected individuals. The purpose of this review is to summarize how innate immune responses may promote tumourigenesis following OV infection and if such responses can be used to predict CCA onset in OV-infected individuals. It also hypothesizes on the role that Helicobacterspp., which are associated with liver fluke infections, may play in activation of the innate the immune system to promote tissue damage and persistent inflammation leading to CCA.<br /> (Copyright © 2018 Elsevier Ltd. All rights reserved.)
- Subjects :
- Animals
Asia, Southeastern
Bile Duct Neoplasms microbiology
Bile Duct Neoplasms parasitology
Cholangiocarcinoma microbiology
Cholangiocarcinoma parasitology
Helicobacter physiology
Helicobacter Infections complications
Humans
Opisthorchiasis microbiology
Bile Duct Neoplasms etiology
Cholangiocarcinoma etiology
Immunity, Innate
Opisthorchiasis complications
Subjects
Details
- Language :
- English
- ISSN :
- 2163-6079
- Volume :
- 101
- Database :
- MEDLINE
- Journal :
- Advances in parasitology
- Publication Type :
- Academic Journal
- Accession number :
- 29907253
- Full Text :
- https://doi.org/10.1016/bs.apar.2018.05.006