title: Expression of selectin ligands on murine effector and IL-10-producing CD4+ T cells from non-infected and infected tissues.
abstract: 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 in vitro studies suggested a correlation between the Th1 phenotype and ligand expression, but whether this also holds true in vivo remained uncertain. We here analyzed selectin ligands on CD4+ T cells producing IFN-gamma, IL-4 or IL-10, prototypic cytokines of the Th1, Th2 and Tr1 subset, respectively. We analyzed mice infected with influenza virus, the bacterium Listeria, and the parasites Toxoplasma (all Th1 models) or Nippostrongylus (Th2 model). A link between the Th1 phenotype and ligand expression was not found in vivo. 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 Nippostrongylus infection. In conclusion, conditions driving T cell polarization into either Th1 or Th2 in vivo 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.
authors.affiliation: Experimentelle Rheumatologie, Medizinische Klinik, Charité Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: Ute
authors.initials: U
authors.lastname: Kretschmer
authors.forename: Kerstin
authors.initials: K
authors.lastname: Bonhagen
authors.forename: Gudrun F
authors.initials: GF
authors.lastname: Debes
authors.forename: Hans-Willi
authors.initials: HW
authors.lastname: Mittrücker
authors.forename: Klaus J
authors.initials: KJ
authors.lastname: Erb
authors.forename: Oliver
authors.initials: O
authors.lastname: Liesenfeld
authors.forename: Dietmar
authors.initials: D
authors.lastname: Zaiss
authors.forename: Thomas
authors.initials: T
authors.lastname: Kamradt
authors.forename: Uta
authors.initials: U
authors.lastname: Syrbe
authors.forename: Alf
authors.initials: A
authors.lastname: Hamann
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016207:Cytokines / Q000276:immunology; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D007156:Immunologic Memory / Q000276:immunology; D009980:Influenza A virus / Q000276:immunology; D016753:Interleukin-10 / Q000096:biosynthesis / Q000276:immunology*; D008024:Ligands; D008088:Listeriosis / Q000276:immunology; D008171:Lung Diseases / Q000276:immunology* / Q000382:microbiology / Q000469:parasitology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009559:Nippostrongylus / Q000276:immunology; D009976:Orthomyxoviridae Infections / Q000276:immunology*; D019087:Selectins / Q000276:immunology / Q000378:metabolism*; D013047:Specific Pathogen-Free Organisms; D017206:Strongylida Infections / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D014123:Toxoplasmosis / Q000276:immunology
chemical_list: D016207:Cytokines; D008024:Ligands; D019087:Selectins; D016753:Interleukin-10