Wang, JunhuaJunhuaWangMüller, Stefan JürgStefan JürgMüllerLin, RenyongRenyongLinSiffert, MyriamMyriamSiffertVuitton, Dominique ADominique AVuittonWen, HaoHaoWenGottstein, BrunoBrunoGottstein0000-0003-0782-37232025-01-082025-01-082017-12https://boris-portal.unibe.ch/handle/20.500.12422/199733INTRODUCTION The growth potential of the tumor-like Echinococcus multilocularis metacestode (causing alveolar echinococcosis, AE) is directly linked to the nature/function of the periparasitic host immune-mediated processes. Previous studies had shown that regulatory T cells (Tregs) become gradually up-regulated in the course of both chronic human and murine AE. Thus we now tackled the role of FoxP3+ Tregs and FoxP3+ -Treg-regulated immune response in contributing to the control of this helminthic infection. METHODS The infection outcome in E. multilocularis-infected DEREG mice was measured upon determining parasite load (wet weight of parasitic metacestode tissue). Flow cytometry and qRT-PCR were used to assess Treg, Th17-, Th1-, Th2-type immune responses and antigen presenting cell activation. RESULTS We showed that E. multilocularis-infected DEREG-mice treated with DT (as compared to infected control DEREG-mice without DT application) exhibited a significantly lower parasite load, associated with a persisting capacity of co-stimulation, and an increased Th1/Th17-polarization. CONCLUSIONS FoxP3+ Tregs appear as one of the key players in immune regulatory processes favoring (i) metacestode survival by inhibiting the maturation potential of co-stimulatory activity and (ii) T cell exhaustion (suppressing Th1/Th17-type immune responses). We showed as well that prospectively, targeting FoxP3+ Tregs could be an option to develop an immunotherapy against AE.enCD4+ CD25+ Treg Echinococcus multilocularis Foxp3 Th1/Th17 immunity co-stimulation600 - Technology::630 - Agriculture500 - Science500 - Science::570 - Life sciences; biologyarticle10.7892/boris.1115572862103410.1002/iid3.181