Phythian-Adams, Alexander T and Cook, Peter C and Lundie, Rachel J and Jones, Lucy H and Smith, Katherine A and Barr, Tom A and Hochweller, Kristin and Anderton, Stephen M and Hämmerling, Günter J and Maizels, Rick M and MacDonald, Andrew S (2010) CD11c depletion severely disrupts Th2 induction and development in vivo. The Journal of experimental medicine, 207 (10). pp. 2089-2096. ISSN 0022-1007
Full text not available from this repository.Abstract
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-γ 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.