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CD11c depletion severely disrupts Th2 induction and development in vivo

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: 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: 25 Oct 2022 08:24
URI: https://orca.cardiff.ac.uk/id/eprint/52733

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