Beschreibung:
<jats:title>Abstract</jats:title><jats:p>Endothelial selectins are crucial for the recruitment of leukocytes into sites of inflammation. On T cells, ligands for selectins become induced upon differentiation into the effector/memory stage. Initial <jats:italic>in vitro</jats:italic> studies suggested a correlation between the Th1 phenotype and ligand expression, but whether this also holds true <jats:italic>in vivo </jats:italic>remained uncertain. We here analyzed selectin ligands on CD4<jats:sup>+</jats:sup> T cells producing IFN‐γ, IL‐4 or IL‐10, prototypic cytokines of the Th1, Th2 and Tr1 subset, respectively. We analyzed mice infected with influenza virus, the bacterium <jats:italic>Listeria,</jats:italic> and the parasites <jats:italic>Toxoplasma</jats:italic> (all Th1 models) or <jats:italic>Nippostrongylus</jats:italic> (Th2 model). A link between the Th1 phenotype and ligand expression was not found <jats:italic>in vivo</jats:italic>. Surprisingly, the potentially regulatory IL‐10‐producing T cells displayed the highest frequency of ligand‐positive cells in general. Within the inflamed tissues, the frequencies of P‐selectin‐binding cells increased in the dominant subset, either Th1 or Th2. Up‐regulation was also found for E‐selectin ligands during influenza, but not <jats:italic>Nippostrongylus</jats:italic> infection. In conclusion, conditions driving T cell polarization into either Th1 or Th2 <jats:italic>in vivo</jats:italic> do not affect the expression of selectin ligands, but acquisition of P‐selectin binding and hence migration into inflamed tissues is boosted by an inflammatory milieu.</jats:p>