| First Author | Phythian-Adams AT | Year | 2010 |
| Journal | J Exp Med | Volume | 207 |
| Issue | 10 | Pages | 2089-96 |
| PubMed ID | 20819926 | Mgi Jnum | J:194809 |
| Mgi Id | MGI:5474755 | Doi | 10.1084/jem.20100734 |
| Citation | Phythian-Adams AT, et al. (2010) CD11c depletion severely disrupts Th2 induction and development in vivo. J Exp Med 207(10):2089-96 |
| abstractText | Although dendritic cells (DCs) are adept initiators of CD4(+) T cell responses, their fundamental importance in this regard in Th2 settings remains to be demonstrated. We have used CD11c-diphtheria toxin (DTx) receptor mice to deplete CD11c(+) cells during the priming stage of the CD4(+) Th2 response against the parasitic helminth Schistosoma mansoni. DTx treatment significantly depleted CD11c(+) DCs from all tissues tested, with 70-80% efficacy. Even this incomplete depletion resulted in dramatically impaired CD4(+) T cell production of Th2 cytokines, altering the balance of the immune response and causing a shift toward IFN-gamma production. In contrast, basophil depletion using Mar-1 antibody had no measurable effect on Th2 induction in this system. These data underline the vital role that CD11c(+) antigen-presenting cells can play in orchestrating Th2 development against helminth infection in vivo, a response that is ordinarily balanced so as to prevent the potentially damaging production of inflammatory cytokines. |
