| First Author | Gold MJ | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 1 | Pages | 122-30 |
| PubMed ID | 26518471 | Mgi Jnum | J:234448 |
| Mgi Id | MGI:5790025 | Doi | 10.1002/eji.201545628 |
| Citation | Gold MJ, et al. (2016) Dendritic-cell expression of Ship1 regulates Th2 immunity to helminth infection in mice. Eur J Immunol 46(1):122-30 |
| abstractText | In mouse models of infection with the gastrointestinal parasite Trichuris muris, appropriate dendritic-cell (DC) Ag sampling, migration, and presentation to T cells are necessary to mount a protective Th2-polarized adaptive immune response, which is needed to clear infection. SH2-containing inositol 5'-phosphatase 1 (SHIP-1) has been shown to be an important regulator of DC function in vitro through the negative regulation of the phosphoinositide 3-kinase (PI3K) pathway, but its role in vivo is relatively unexplored. In the current work, mice with a specific deletion of SHIP-1 in DCs (Ship1(DeltaDC) ) were infected with the parasite T. muris. Ship1(DeltaDC) mice were susceptible to infection due to ineffective priming of Th2-polarized responses. This is likely due to an increased production of interleukin (IL) 12p40 by SHIP-1-deficient DCs, as in vivo antibody blockade of IL-12p40 was able to facilitate the clearing of infection in Ship1(DeltaDC) mice. Our results describe a critical role for SHIP-1 in regulating the ability of DCs to efficiently prime Th2-type responses. |
