| First Author | Kane CM | Year | 2008 |
| Journal | Infect Immun | Volume | 76 |
| Issue | 12 | Pages | 5754-9 |
| PubMed ID | 18824534 | Mgi Jnum | J:143320 |
| Mgi Id | MGI:3826694 | Doi | 10.1128/IAI.00497-08 |
| Citation | Kane CM, et al. (2008) Schistosoma mansoni egg antigen-mediated modulation of Toll-like receptor (TLR)-induced activation occurs independently of TLR2, TLR4, and MyD88. Infect Immun 76(12):5754-9 |
| abstractText | 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 naive mice. |
