| Literature DB >> 22535180 |
S Hadidi1, F Antignano, M R Hughes, S K H Wang, K Snyder, G M Sammis, W G Kerr, K M McNagny, C Zaph.
Abstract
Helminth infection leads to the local proliferation and accumulation of macrophages in tissues. However, the function of macrophages during helminth infection remains unclear. SH2-containing inositol 5'-phosphatase 1 (Ship1, Inpp5d) is a lipid phosphatase that has been shown to play a critical role in macrophage function. Here, we identify a critical role for Ship1 in the negative regulation of interleukin (IL)-12/23p40 production by macrophages during infection with the intestinal helminth parasite Trichuris muris. Mice with myeloid cell-specific deletion of Ship1 (Ship1(ΔLysM) mice) develop a non-protective T-helper type 1 cell response and fail to expel parasites. Ship1-deficient macrophages produce heightened levels of IL-12/23p40 in vitro and in vivo and antibody blockade of IL-12/23p40 renders Ship1(ΔLysM) mice resistant to Trichuris infection. Our results identify a critical role for the negative regulation of IL-12/23p40 production by macrophages in the development of a protective T(H)2 cell response.Entities:
Mesh:
Substances:
Year: 2012 PMID: 22535180 DOI: 10.1038/mi.2012.29
Source DB: PubMed Journal: Mucosal Immunol ISSN: 1933-0219 Impact factor: 7.313