Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Oct 28, 2017; 9(30): 1176-1189
Published online Oct 28, 2017. doi: 10.4254/wjh.v9.i30.1176
Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review
Nikica M Grubor, Katica D Jovanova-Nesic, Yehuda Shoenfeld
Nikica M Grubor, Department of Hepatobiliary and Pancreatic Surgery, First Surgical University Hospital, Clinical Center of Serbia, School of Medicine University of Belgrade, 11000 Belgrade, Serbia
Katica D Jovanova-Nesic, Immunology Research Center, Institute of Virology, Vaccine and Sera-Torlak, 11221 Belgrade, Serbia
Katica D Jovanova-Nesic, European Center for Peace and Development, University for Peace in the United Nation established in Belgrade, 11000 Belgrade, Serbia
Yehuda Shoenfeld, Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel Aviv University, 5265601 Tel-Hashomer, Tel Aviv, Israel
Author contributions: All the authors reviewed the literature and wrote the manuscript; Shoenfeld Y edited the paper.
Conflict-of-interest statement: No potential conflicts of interest.
Open-Access: 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:
Correspondence to: Katica D Jovanova-Nesic, PhD, Immunology Research Center, Institute of Virology, Vaccine and Sera-Torlak, Vojvode Stepe 458, 11221 Belgrade, Serbia.
Telephone: +381-11-3948381 Fax: +381-11-3234082
Received: March 25, 2017
Peer-review started: March 28, 2017
First decision: June 30, 2017
Revised: August 28, 2017
Accepted: September 14, 2017
Article in press: September 15, 2017
Published online: October 28, 2017

Cystic echinococcosis (CE) is an infectious disease caused by the larvae of parasite Echinococcus granulosus (E. granulosus). To successfully establish an infection, parasite release some substances and molecules that can modulate host immune functions, stimulating a strong anti-inflammatory reaction to carry favor to host and to reserve self-survival in the host. The literature was reviewed using MEDLINE, and an open access search for immunology of hydatidosis was performed. Accumulating data from animal experiments and human studies provided us with exciting insights into the mechanisms involved that affect all parts of immunity. In this review we used the existing scientific data and discuss how these findings assisted with a better understanding of the immunology of E. granulosus infection in man. The aim of this study is to point the several facts that challenge immune and autoimmune responses to protect E. granulosus from elimination and to minimize host severe pathology. Understanding the immune mechanisms of E. granulosus infection in an intermediate human host will provide, we believe, a more useful treatment with immunomodulating molecules and possibly better protection from parasitic infections. Besides that, the diagnosis of CE has improved due to the application of a new molecular tool for parasite identification by using of new recombinant antigens and immunogenic peptides. More studies for the better understanding of the mechanisms of parasite immune evasion is necessary. It will enable a novel approach in protection, detection and improving of the host inflammatory responses. In contrast, according to the “hygiene hypothesis”, clinical applications that decrease the incidence of infection in developed countries and recently in developing countries are at the origin of the increasing incidence of both allergic and autoimmune diseases. Thus, an understanding of the immune mechanisms of E. granulosus infection is extremely important.

Keywords: Lymphocytes, Dendritic cells, Immunity, Autoimmunity, Cytokines, Echinococcus granulosus

Core tip: The most common location of a hydatid echinococcal cyst is in the liver. The survival of Echinococcus within host tissues, despite the development of specific antibodies, is possible due to specific immunomodulation induced by parasites. Perpetual survival of parasites indicating multi-level systematic evasion against host protective reaction to persist their growth and spreading. Complement modulation, a metabolic adaptation to the host microenvironment, plentiful thermostable immunogenic antigen B in the cystic fluid, and induction of CD4+CD8+FOXP3+ T cells allows the persistence of the parasites. Parasites influence dendritic cell (DC) maturation and impair activation by toll-like receptor. It seems that DC-parasite interaction is pivotal in triggering and regulating parasite induced immunity.