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      IRF4 Transcription Factor-Dependent CD11b + Dendritic Cells in Human and Mouse Control Mucosal IL-17 Cytokine Responses

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          Summary

          Mouse and human dendritic cells (DCs) are composed of functionally specialized subsets, but precise interspecies correlation is currently incomplete. Here, we showed that murine lung and gut lamina propria CD11b + DC populations were comprised of two subsets: FLT3- and IRF4-dependent CD24 +CD64 DCs and contaminating CSF-1R-dependent CD24 CD64 + macrophages. Functionally, loss of CD24 +CD11b + DCs abrogated CD4 + T cell-mediated interleukin-17 (IL-17) production in steady state and after Aspergillus fumigatus challenge. Human CD1c + DCs, the equivalent of murine CD24 +CD11b + DCs, also expressed IRF4, secreted IL-23, and promoted T helper 17 cell responses. Our data revealed heterogeneity in the mouse CD11b + DC compartment and identifed mucosal tissues IRF4-expressing DCs specialized in instructing IL-17 responses in both mouse and human. The demonstration of mouse and human DC subsets specialized in driving IL-17 responses highlights the conservation of key immune functions across species and will facilitate the translation of mouse in vivo findings to advance DC-based clinical therapies.

          Highlights

          • Mucosal CD11b + DCs consist of CD24 +CD64 DCs and CD24 CD64 + macrophages
          • Mucosal CD24 +CD11b + DCs are IRF4-dependent
          • IRF4-dependent CD24 +CD11b + DCs secrete IL-23α and control mucosal IL-17 responses
          • Human CD1c +CD11b + DCs are functional homologs of murine CD24 +CD11b + DCs

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          Author and article information

          Contributors
          Journal
          Immunity
          Immunity
          Immunity
          Cell Press
          1074-7613
          1097-4180
          23 May 2013
          23 May 2013
          : 38
          : 5
          : 970-983
          Affiliations
          [1 ]Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A *STAR), 138648 Singapore
          [2 ]Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
          [3 ]Department of Immunology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan
          [4 ]II Medical Department, Klinikum Rechts der Isar, Technical University Munich, Ismaninger Strasse 22, 81675 Munich, Germany
          [5 ]National University Hospital, Singapore 119074, Singapore
          [6 ]Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119077, Singapore
          [7 ]Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
          [8 ]Singapore Institute for Clinical Sciences, Agency for Science, Technology and Research (A *STAR), Singapore 529825, Singapore
          Author notes
          [9]

          These authors contributed equally to this work

          Article
          IMMUNI2602
          10.1016/j.immuni.2013.04.011
          3666057
          23706669
          © 2013 ELL & Excerpta Medica.

          This document may be redistributed and reused, subject to certain conditions.

          Categories
          Article

          Immunology

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