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    <title>Kimman, T.G.</title>
    <link>http://repub.eur.nl/res/aut/779/</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>Respiratory syncytial virus differentially activates murine myeloid and plasmacytoid dendritic cells (Article)</title>
      <link>http://repub.eur.nl/res/pub/35228/</link>
      <pubDate>2007-09-01T00:00:00Z</pubDate>
      <description>Respiratory syncytial virus (RSV) is the primary cause of bronchiolitis in young children. Upon infection both T helper 1 (Th1) and Th2 cytokines are produced. Because RSV-induced Th2 responses have been associated with severe immunopathology and aggravation of allergic reactions, the regulation of the immune response following RSV infection is crucial. In this study we examined the influence of RSV on the activation and function of murine bone marrow-derived dendritic cells (DCs). RSV induced the expression of maturation markers on myeloid DCs (mDCs) in vitro. The mDCs stimulated with RSV and ovalbumin (OVA) enhanced proliferation of OVA-specific T cells, which produced both Th1 and Th2 cytokines. In contrast to mDCs, RSV did not induce the expression of maturation markers on plasmacytoid DCs (pDCs), not did it enhance the proliferation of OVA-specific T cells that were cocultured with pDCs. However, RSV stimulated the production of interferon-α (IFN-α) by pDCs. Our findings indicate a clear difference in the functional activation of DC subsets. RSV-stimulated mDCs may have immunostimulatory effects on both Th1 and Th2 responses, while RSV-stimulated pDCs have direct antiviral activity through the release of IFN-α. </description>
    </item> <item>
      <title>Timing of infection and prior immunization with respiratory syncytial virus (RSV) in RSV-enhanced allergic inflammation (Article)</title>
      <link>http://repub.eur.nl/res/pub/3970/</link>
      <pubDate>2004-05-15T00:00:00Z</pubDate>
      <description>Respiratory syncytial virus (RSV) infection has been shown to be a risk factor for the development of allergy in humans and mice. The allergy-enhancing properties of RSV may be dependent on atopic background and an individual's history of RSV infection. We examined the influence of the timing of infection and prior inoculation with RSV in a mouse model of allergic asthma. Mice were sensitized to and challenged with ovalbumin (OVA) and were inoculated with RSV either before or during the sensitization or challenge period. One group of mice was inoculated with RSV both before sensitization to OVA and during challenge with OVA. Increased pulmonary expression of interleukin (IL)-4, IL-5, and IL-13 mRNA and aggravated alveolitis and hypertrophy of mucus-producing cells were observed only when OVA-sensitized mice were inoculated with RSV shortly before or during challenge with OVA. Despite protection against viral replication, prior inoculation with RSV did not abrogate RSV-enhanced, OVA-induced expression of T helper 2 (Th2) cytokines in the lung. In conclusion, inoculation with RSV enhances allergic disease only when the immune system has already been Th2-primed by the allergen (i.e., OVA). This RSV-enhanced allergy is not completely abrogated by prior inoculation with RSV.</description>
    </item> <item>
      <title>Antigenic and molecular heterogeneity in recent swine influenza A(H1N1) virus isolates with possible implications for vaccination policy. (Article)</title>
      <link>http://repub.eur.nl/res/pub/3802/</link>
      <pubDate>2001-08-14T00:00:00Z</pubDate>
      <description>In order to explore the occurrence of antigenic drift in swine influenza A(H1N1) viruses and the match between epidemic and vaccine strains, 26 virus isolates from outbreaks of respiratory disease among finishing pigs in the Netherlands in the 1995/1996 season and reference strains from earlier outbreaks were examined using serological and molecular methods. In contrast to swine H3N2 viruses, no significant antigenic drift was observed in swine H1N1 viruses isolated from the late 1980s up to 1996 inclusive. However, a marked antigenic and genetic heterogeneity in haemagglutination inhibition tests and nucleotide sequence analyses was detected among the 26 recent swine H1N1 virus strains. Interestingly, the observed antigenic and molecular variants were not randomly distributed over the farms. This finding indicates independent introductions of different swine H1N1 virus variants at the various farms of the study and points to a marked difference between the epidemiologies of human and swine influenza viruses. The observed heterogeneity may hamper the control of swine influenza by vaccination and indicates that the efficacy of current swine influenza vaccines requires re-evaluation and that the antigenic reactivity of swine influenza viruses should be monitored on a regular basis.</description>
    </item> <item>
      <title>Antigenic drift in swine influenza H3 haemagglutinins with implications for vaccination policy. (Article)</title>
      <link>http://repub.eur.nl/res/pub/3669/</link>
      <pubDate>1999-03-01T00:00:00Z</pubDate>
      <description>In order to explore the occurrence of antigenic drift in swine influenza A(H3N2) virus, we examined virus strains from outbreaks of respiratory disease among finishing pigs in the Netherlands in 1996 and 1997 and from earlier outbreaks. In contrast to swine H3N2 strains from the 1980s, the recent isolates did not show significant cross-reactivity with human influenza A(H3N2) viruses from 1972-1975 in haemagglutination inhibition tests. These new strains form a separate branch in the phylogenetic trec of the HA1 parts of HA. We conclude that recently there has been considerable antigenic drift within the swine H3N2 viruses in the Netherlands and Belgium and recommend replacement of the A/Port Chalmers/1/73 (H3N2) strain in the current vaccine by a more recent swine H3N2 isolate.</description>
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