Phythian-Adams, A. T., Cook, P. C., Lundie, R. J., Jones, L. H., Smith, Katherine A. ORCID: https://orcid.org/0000-0001-8150-5702, Barr, T. A., Hochweller, K., Anderton, S. M., Hammerling, G. J., Maizels, R. M. and MacDonald, A. S.
2010.
CD11c depletion severely disrupts Th2 induction and development in vivo.
Journal of Experimental Medicine
207
(10)
, pp. 2089-2096.
10.1084/jem.20100734
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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.
| Item Type: | Article |
|---|---|
| Date Type: | Publication |
| Status: | Published |
| Schools: | Schools > Medicine |
| Subjects: | Q Science > QH Natural history > QH426 Genetics R Medicine > R Medicine (General) |
| Publisher: | Rockefeller University Press |
| ISSN: | 0022-1007 |
| Date of First Compliant Deposit: | 30 March 2016 |
| Last Modified: | 22 May 2023 06:29 |
| URI: | https://orca.cardiff.ac.uk/id/eprint/52733 |
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