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CD11c depletion severely disrupts Th2 induction and development in vivo

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 respons...

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Autores principales: Phythian-Adams, Alexander T., Cook, Peter C., Lundie, Rachel J., Jones, Lucy H., Smith, Katherine A., Barr, Tom A., Hochweller, Kristin, Anderton, Stephen M., Hämmerling, Günter J., Maizels, Rick M., MacDonald, Andrew S.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947067/
https://www.ncbi.nlm.nih.gov/pubmed/20819926
http://dx.doi.org/10.1084/jem.20100734
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author Phythian-Adams, Alexander T.
Cook, Peter C.
Lundie, Rachel J.
Jones, Lucy H.
Smith, Katherine A.
Barr, Tom A.
Hochweller, Kristin
Anderton, Stephen M.
Hämmerling, Günter J.
Maizels, Rick M.
MacDonald, Andrew S.
author_facet Phythian-Adams, Alexander T.
Cook, Peter C.
Lundie, Rachel J.
Jones, Lucy H.
Smith, Katherine A.
Barr, Tom A.
Hochweller, Kristin
Anderton, Stephen M.
Hämmerling, Günter J.
Maizels, Rick M.
MacDonald, Andrew S.
author_sort Phythian-Adams, Alexander T.
collection PubMed
description 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.
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spelling pubmed-29470672011-03-27 CD11c depletion severely disrupts Th2 induction and development in vivo Phythian-Adams, Alexander T. Cook, Peter C. Lundie, Rachel J. Jones, Lucy H. Smith, Katherine A. Barr, Tom A. Hochweller, Kristin Anderton, Stephen M. Hämmerling, Günter J. Maizels, Rick M. MacDonald, Andrew S. J Exp Med Brief Definitive Report 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. The Rockefeller University Press 2010-09-27 /pmc/articles/PMC2947067/ /pubmed/20819926 http://dx.doi.org/10.1084/jem.20100734 Text en © 2010 Phythian-Adams et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Brief Definitive Report
Phythian-Adams, Alexander T.
Cook, Peter C.
Lundie, Rachel J.
Jones, Lucy H.
Smith, Katherine A.
Barr, Tom A.
Hochweller, Kristin
Anderton, Stephen M.
Hämmerling, Günter J.
Maizels, Rick M.
MacDonald, Andrew S.
CD11c depletion severely disrupts Th2 induction and development in vivo
title CD11c depletion severely disrupts Th2 induction and development in vivo
title_full CD11c depletion severely disrupts Th2 induction and development in vivo
title_fullStr CD11c depletion severely disrupts Th2 induction and development in vivo
title_full_unstemmed CD11c depletion severely disrupts Th2 induction and development in vivo
title_short CD11c depletion severely disrupts Th2 induction and development in vivo
title_sort cd11c depletion severely disrupts th2 induction and development in vivo
topic Brief Definitive Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947067/
https://www.ncbi.nlm.nih.gov/pubmed/20819926
http://dx.doi.org/10.1084/jem.20100734
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