| First Author | Sallmann E | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 1 | Pages | 164-71 |
| PubMed ID | 21622859 | Mgi Jnum | J:175939 |
| Mgi Id | MGI:5287952 | Doi | 10.4049/jimmunol.1003392 |
| Citation | Sallmann E, et al. (2011) High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation. J Immunol 187(1):164-71 |
| abstractText | The IgE-mediated and Th2-dependent late-phase reaction remains a mechanistically enigmatic and daunting element of human allergic inflammation. In this study, we uncover the FcepsilonRI on dendritic cells (DCs) as a key in vivo component of this form of allergy. Because rodent, unlike human, DCs lack FcepsilonRI, this mechanism could be revealed only by using a new transgenic mouse model with human-like FcepsilonRI expression on DCs. In the presence of IgE and allergen, FcepsilonRI(+) DCs instructed naive T cells to differentiate into Th2 cells in vitro and boosted allergen-specific Th2 responses and Th2-dependent eosinophilia at the site of allergen exposure in vivo. Thus, FcepsilonRI on DCs drives the cascade of pathogenic reactions linking the initial allergen capture by IgE with subsequent Th2-dominated T cell responses and the development of late-phase allergic tissue inflammation. |
