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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., 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: 04 Jun 2017 05:40
URI: http://orca.cf.ac.uk/id/eprint/52733

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