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Secreted Proteins from the Helminth Fasciola hepatica Inhibit the Initiation of Autoreactive T Cell Responses and Prevent Diabetes in the NOD Mouse
Authors
A Cooke
A Espinoza-Jiménez
+59 more
Andrew T. Hutchinson
Ann M. Simpson
B Calderon
Bronwyn A. O'Brien
C Alam
C Schebesch
DG Alleva
DJ Dowling
DW Dunne
FD Finkelman
H Okada
HJ Hernandez
HS Jun
I Jaakkola
J Correale
John P. Dalton
JP Hewitson
K Kodama
KA Saunders
KP Walsh
Lucienne Chatenoud
M McKenna
Maria E. Lund
Mark W. Robinson
MH Abdulla
MJ Broadhurst
MP Hubner
MS Wilson
MW Robinson
MW Robinson
NM Boukli
OT Burton
P Loke
P Zaccone
P Zaccone
P Zaccone
P Zaccone
P Zaccone
PK Mishra
Q Liu
R Parsa
RM Anthony
RM Maizels
RW Summers
RW Summers
S Donnelly
S Donnelly
S Donnelly
S Hussain
S Steinfelder
SD Bilbo
Sheila Donnelly
SJ Turley
SM O'Neill
V Aravindhan
V Gillan
W Gaisford
W Harnett
Y Osada
Publication date
1 January 2014
Publisher
'Public Library of Science (PLoS)'
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PubMed
Abstract
Infections with helminth parasites prevent/attenuate auto-inflammatory disease. Here we show that molecules secreted by a helminth parasite could prevent Type 1 Diabetes (T1D) in nonobese diabetic (NOD) mice. When delivered at 4 weeks of age (coincident with the initiation of autoimmunity), the excretory/secretory products of Fasciola hepatica (FhES) prevented the onset of T1D, with 84% of mice remaining normoglycaemic and insulitis-free at 30 weeks of age. Disease protection was associated with suppression of IFN-γ secretion from autoreactive T cells and a switch to the production of a regulatory isotype (from IgG2a to IgG1) of autoantibody. Following FhES injection, peritoneal macrophages converted to a regulatory M2 phenotype, characterised by increased expression levels of Ym1, Arg-1, TGFb and PD-L1. Expression of these M2 genetic markers increased in the pancreatic lymph nodes and the pancreas of FhES-treated mice. In vitro , FhES-stimulated M2 macrophages induced the differentiation of Tregs from splenocytes isolated from naïve NOD mice. Collectively, our data shows that FhES contains immune-modulatory molecules that mediate protection from autoimmune diabetes via the induction and maintenance of a regulatory immune environment. © 2014 Lund et al
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