Critical role for syndecan-4 in dendritic cell migration during development of allergic airway inflammation

Tobias Polte (), Susanne Petzold, Jessica Bertrand, Nicole Schütze, Denise Hinz, Jan C. Simon, Irina Lehmann, Frank Echtermeyer, Thomas Pap and Marco Averbeck
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Tobias Polte: UFZ—Helmholtz Centre for Environmental Research Leipzig-Halle, Permoserstrasse 15, Leipzig 04318, Germany
Susanne Petzold: UFZ—Helmholtz Centre for Environmental Research Leipzig-Halle, Permoserstrasse 15, Leipzig 04318, Germany
Jessica Bertrand: Institute for Experimental Musculoskeletal Medicine, University Hospital Münster
Nicole Schütze: UFZ—Helmholtz Centre for Environmental Research Leipzig-Halle, Permoserstrasse 15, Leipzig 04318, Germany
Denise Hinz: Venerology and Allergology, Leipzig University Medical Center
Jan C. Simon: Venerology and Allergology, Leipzig University Medical Center
Irina Lehmann: UFZ—Helmholtz Centre for Environmental Research Leipzig-Halle, Permoserstrasse 15, Leipzig 04318, Germany
Frank Echtermeyer: Hannover Medical School
Thomas Pap: Institute for Experimental Musculoskeletal Medicine, University Hospital Münster
Marco Averbeck: Venerology and Allergology, Leipzig University Medical Center

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract Syndecan-4 (SDC4), expressed on dendritic cells (DCs) and activated T cells, plays a crucial role in DC motility and has been shown as a potential target for activated T-cell-driven diseases. In the present study, we investigate the role of SDC4 in the development of T-helper 2 cell-mediated allergic asthma. Using SDC4-deficient mice or an anti-SDC4 antibody we show that the absence or blocking of SDC4 signalling in ovalbumin-sensitized mice results in a reduced asthma phenotype compared with control animals. Most importantly, even established asthma is significantly decreased using the anti-SDC4 antibody. The disturbed SDC4 signalling leads to an impaired motility and directional migration of antigen-presenting DCs and therefore, to a modified sensitization leading to diminished airway inflammation. Our results demonstrate that SDC4 plays an important role in asthma induction and indicate SDC4 as possible target for therapeutic intervention in this disease.

Date: 2015
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DOI: 10.1038/ncomms8554

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