<?xml version="1.0" encoding="UTF-8" standalone="no" ?>
<rss version="2.0">
  <channel>
    <title>Gutierrez-Ramos, J.C.</title>
    <link>http://repub.eur.nl/res/aut/7843/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Myeloid dendritic cells induce Th2 responses to inhaled antigen, leading to eosinophilic airway inflammation (Article)</title>
      <link>http://repub.eur.nl/res/pub/9442/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>The aim of this study was to investigate whether dendritic cells (DCs) can
          induce sensitization to aeroallergen in a mouse model of allergic asthma.
          Ovalbumin-pulsed (OVA-pulsed) or unpulsed myeloid DCs that were injected
          into the airways of naive mice migrated into the mediastinal lymph nodes.
          When challenged 2 weeks later with an aerosol of OVA, activated CD4 and
          CD8 lymphocytes, eosinophils, and neutrophils were recruited to the lungs
          of actively immunized mice. These CD4(+) lymphocytes produced
          predominantly IL-4 and IL-5 but also IFN-gamma, whereas CD8(+) lymphocytes
          produced predominantly IFN-gamma. Histological analysis revealed
          perivascular and peribronchial eosinophilic infiltrates and goblet cell
          hyperplasia. Studies in IL-4(-/-) and CD28(-/-) mice revealed that
          production of IL-4 by host cells and provision of costimulation to T cells
          by DCs were critical for inducing the response. Lung CD4(+) T cells
          strongly expressed the Th2 marker T1/ST2, and signaling through this
          molecule via a ligand expressed on DCs was essential for the establishment
          of airway eosinophilia. These data demonstrate that DCs in the airways
          induce sensitization to inhaled antigen and that molecules expressed on
          the surface of these cells are critical for the development of
          Th2-dependent airway eosinophilia.</description>
    </item>
  </channel>
</rss>