Helminth antigens modulate TLR-initiated dendritic cell activation

Colleen M. Kane, Laura Cervi, Jie Sun, Amy S. McKee, Katherine S. Masek, Sagi Shapira, Christopher A. Hunter, Edward J. Pearce

Research output: Contribution to journalArticlepeer-review

195 Scopus citations


There is increasing awareness that helminth infections can ameliorate proinflammatory conditions. In part, this is due to their inherent ability to induce Th2 and, perhaps, regulatory T cell responses. However, recent evidence indicates that helminths also have direct anti-inflammatory effects on innate immune responses. In this study, we address this issue and show that soluble molecules from the eggs of the helminth parasite Schistosoma mansoni (SEA) suppress LPS-induced activation of immature murine dendritic cells, including MHC class II, costimulatory molecule expression, and IL-12 production. SEA-augmented LPS-induced production of IL-10 is in part responsible for the observed reduction in LPS-induced IL-12 production. However, analyses of IL-10-/- DC revealed distinct IL-10-independent suppressive effects of SEA. IL-10-independent mechanisms are evident in the suppression of TLR ligand-induced MAPK and NF-κB signaling pathways. Microarray analyses demonstrate that SEA alone uniquely alters the expression of a small subset of genes that are not up-regulated during conventional TLR-induced DC maturation. In contrast, the effects of SEA on TLR ligand-induced DC activation were striking: when mixed with LPS, SEA significantly affects the expression of >100 LPS-regulated genes. These findings indicate that SEA exerts potent anti-inflammatory effects by directly regulating the ability of DC to respond to TLR ligands.

Original languageEnglish (US)
Pages (from-to)7454-7461
Number of pages8
JournalJournal of Immunology
Issue number12
StatePublished - Dec 15 2004

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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