Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 205, Issue 1, Pages 79-90Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20062027
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- Intramural NIH HHS Funding Source: Medline
- NCI NIH HHS [N01CO12400, N01-CO-12400] Funding Source: Medline
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Eosinophil-derived neurotoxin (EDN) is an eosinophil granule-derived secretory protein with ribonuclease and antiviral activity. We have previously shown that EDN can induce the migration and maturation of dendritic cells (DCs). Here, we report that EDN can activate myeloid DCs by triggering the Toll-like receptor (TLR)2-myeloid differentiation factor 88 signaling pathway, thus establishing EDN as an endogenous ligand of TLR2. EDN activates TLR2 independently of TLR1 or TLR6. When mice were immunized with ovalbumin (OVA) together with EDN or with EDN-treated OVA-loaded DCs, EDN enhanced OVA-specifi c T helper (Th)2-biased immune responses as indicated by predominant production of OVA-specifi c interleukin (IL)-5, IL-6, IL-10, and IL-13, as well as higher levels of immunoglobulin (Ig)G1 than IgG2a. Based on its ability to serve as a chemoattractant and activator of DCs, as well as the capacity to enhance antigen-specifi c immune responses, we consider EDN to have the properties of an endogenous alarmin that alerts the adaptive immune system for preferential enhancement of antigen-specifi c Th2 immune responses.
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