Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 207, Issue 10, Pages 2089-2096Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20100734
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Funding
- National institute for Asthma and Infectious Disease Schistosomiasis Resource Center at the Biomedical Research Institute (Rockville, MD) [N01-AI-30026]
- Medical Research Council UK
- Wellcome Trust
- Medical Research Council [G9900991B, G0801924, G0701437] Funding Source: researchfish
- MRC [G0801924, G0701437] Funding Source: UKRI
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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.
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