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Infection and Immunity, December 2008, p. 5754-5759, Vol. 76, No. 12
0019-9567/08/$08.00+0 doi:10.1128/IAI.00497-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Received 22 April 2008/ Returned for modification 27 May 2008/ Accepted 28 August 2008
Unlike most pathogens, helminth parasites and their products induce strong Th2 responses, and dendritic cells (DCs) and macrophages exposed to helminth antigens generally fail to produce interleukin-12. Rather, it has been shown that helminth products such as soluble egg antigens (SEA; a soluble extract from Schistosoma mansoni eggs) inhibit the activation of DCs in response to classical Toll-like receptor (TLR) ligands such as lipopolysaccharide or CpG. Nevertheless, recent work has suggested that TLR4 and/or TLR2 plays an important role in the recognition of helminth products by DCs and macrophages and in the development of Th2 responses. Using DCs derived from TLR4–/–, TLR2–/–, or MyD88–/– mice, we have demonstrated that the ability of SEA to modulate DC activation is MyD88 independent and requires neither TLR4 nor TLR2. Moreover, TLR2 and TLR4 are not required for SEA-pulsed DCs to induce Th2 responses in naïve mice.
Published ahead of print on 29 September 2008.
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