Innate Immunity

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Macrophages participate in IL-17-mediated inflammation

  1. Jobert G. Barin1,2,
  2. G. Christian Baldeviano2,
  3. Monica V. Talor3,
  4. Lei Wu2,
  5. SuFey Ong2,
  6. Farhan Quader2,
  7. Ping Chen3,4,
  8. Dongfeng Zheng3,
  9. Patrizio Caturegli3,
  10. Noel R. Rose1,2,3,
  11. Daniela C̆iháková3,*

Article first published online: 23 JAN 2012

DOI: 10.1002/eji.201141737

Issue

European Journal of Immunology

European Journal of Immunology

Volume 42, Issue 3, pages 726–736, March 2012

Additional Information

How to Cite

Barin, J. G., Baldeviano, G. C., Talor, M. V., Wu, L., Ong, S., Quader, F., Chen, P., Zheng, D., Caturegli, P., Rose, N. R. and C̆iháková, D. (2012), Macrophages participate in IL-17-mediated inflammation. Eur. J. Immunol., 42: 726–736. doi: 10.1002/eji.201141737

Author Information

  1. 1

    Training Program in Immunology, Johns Hopkins University School of Medicine, Boltimore, MD, USA

  2. 2

    W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA

  3. 3

    Department of Pathology, Division of Immunology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

  4. 4

    Key Laboratory of Viral Heart Diseases, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China

*JHUSOM, Department of Pathology, 720 Rutland Avenue, Baltimore, MD 21205-2109, USA, Fax: +1-410-614-3548

Publication History

  1. Issue published online: 9 APR 2012
  2. Article first published online: 23 JAN 2012
  3. Accepted manuscript online: 12 DEC 2011 05:11AM EST
  4. Manuscript Accepted: 30 NOV 2011
  5. Manuscript Revised: 7 NOV 2011
  6. Manuscript Received: 9 MAY 2011

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Keywords:

  • Interleukin-17;
  • K'xFC;pffer cell;
  • MF;
  • Microglia;
  • Monocyte

Abstract

The involvement of macrophages (MΦs) in Th17-cell responses is still poorly understood. While neutrophils are thought to be the predominant effector of Th17-cell responses, IL-17 is also known to induce myelotropic chemokines and growth factors. Other T-cell-derived cytokines induce non-classical functions, suggesting that IL-17 sigxnaling may similarly elicit unique MΦ functions. Here, we characterized the expression of subunits of the IL-17 receptor on primary murine MΦs from different anatomical compartments. The greatest expression of IL-17 receptors was observed on mucosal Ly6Chi "inflammatory" MΦs. We further observed upregulation of IL-17 receptors in vitro on bone marrow-derived macrophages (BMMΦs) in response to peptidoglycan or CpG oligonucleotide stimuli, and in vivo, upon CFA administration. Macrophages expressing IL-17 receptors were observed infiltrating the hearts of mice with myocarditis, and genetic ablation of IL-17RA altered MΦ recruitment. Treating primary MΦs from a wide variety of different anatomic sources (as well as cell lines) with IL-17A induced the production of unique profiles of cytokines and chemokines, including GM-CSF, IL-3, IL-9, CCL4/MIP-1β and CCL5/RANTES. IL-17A also induced production of IL-12p70; IL-17-signaling-deficient MΦs elicited diminished IFN-γ production by responding DO11.10 CD4+ T cells when used as APCs. These data indicate that MΦs from different anatomic locations direct IL-17-mediated responses.

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