TY - JOUR
T1 - Eosinophil-derived IL-10 supports chronic nematode infection
AU - Huang, Lu
AU - Gebreselassie, Nebiat G.
AU - Gagliardo, Lucille F.
AU - Ruyechan, Maura C.
AU - Lee, Nancy A.
AU - Lee, James J.
AU - Appleton, Judith A.
N1 - Publisher Copyright:
Copyright © 2014 by The American Association of Immunologists, Inc.
PY - 2014/10/15
Y1 - 2014/10/15
N2 - Eosinophilia is a feature of the host immune response that distinguishes parasitic worms from other pathogens, yet a discrete function for eosinophils in worm infection has been elusive. The aim of this study was to clarify the mechanism(s) underlying the striking and unexpected observation that eosinophils protect intracellular, muscle-stage Trichinella spiralis larvae against NO-mediated killing. Our findings indicate that eosinophils are specifically recruited to sites of infection at the earliest stage of muscle infection, consistent with a local response to injury. Early recruitment is essential for larval survival. By producing IL-10 at the initiation of infection, eosinophils expand IL-10+ myeloid dendritic cells and CD4+ IL-10+ T lymphocytes that inhibit inducible NO synthase (iNOS) expression and protect intracellular larvae. The results document a novel immunoregulatory function of eosinophils in helminth infection, in which eosinophil-derived IL-10 drives immune responses that eventually limit local NO production. In this way, the parasite co-opts an immune response in a way that enhances its own survival.
AB - Eosinophilia is a feature of the host immune response that distinguishes parasitic worms from other pathogens, yet a discrete function for eosinophils in worm infection has been elusive. The aim of this study was to clarify the mechanism(s) underlying the striking and unexpected observation that eosinophils protect intracellular, muscle-stage Trichinella spiralis larvae against NO-mediated killing. Our findings indicate that eosinophils are specifically recruited to sites of infection at the earliest stage of muscle infection, consistent with a local response to injury. Early recruitment is essential for larval survival. By producing IL-10 at the initiation of infection, eosinophils expand IL-10+ myeloid dendritic cells and CD4+ IL-10+ T lymphocytes that inhibit inducible NO synthase (iNOS) expression and protect intracellular larvae. The results document a novel immunoregulatory function of eosinophils in helminth infection, in which eosinophil-derived IL-10 drives immune responses that eventually limit local NO production. In this way, the parasite co-opts an immune response in a way that enhances its own survival.
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U2 - 10.4049/jimmunol.1400852
DO - 10.4049/jimmunol.1400852
M3 - Article
C2 - 25210122
AN - SCOPUS:84907487371
SN - 0022-1767
VL - 193
SP - 4178
EP - 4187
JO - Journal of Immunology
JF - Journal of Immunology
IS - 8
ER -