Expression of selectin ligands on murine effector and IL-10-producing CD4+ T cells from non-infected and infected tissues

TY - JOUR

T1 - Expression of selectin ligands on murine effector and IL-10-producing CD4+ T cells from non-infected and infected tissues

AU - Kretschmer, Ute

AU - Bonhagen, Kerstin

AU - Debes, Gudrun F

AU - Mittrücker, Hans-Willi

AU - Erb, Klaus J

AU - Liesenfeld, Oliver

AU - Zaiss, Dietmar

AU - Kamradt, Thomas

AU - Syrbe, Uta

AU - Hamann, Alf

PY - 2004/11/1

Y1 - 2004/11/1

N2 - 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.

AB - 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.

KW - Animals

KW - CD4-Positive T-Lymphocytes

KW - Cytokines

KW - Female

KW - Gene Expression Regulation

KW - Immunologic Memory

KW - Influenza A virus

KW - Interleukin-10

KW - Ligands

KW - Listeriosis

KW - Lung Diseases

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Nippostrongylus

KW - Orthomyxoviridae Infections

KW - Selectins

KW - Specific Pathogen-Free Organisms

KW - Strongylida Infections

KW - T-Lymphocytes, Regulatory

KW - Toxoplasmosis

U2 - 10.1002/eji.200424972

DO - 10.1002/eji.200424972

M3 - SCORING: Journal article

C2 - 15384048

VL - 34

SP - 3070

EP - 3081

JO - EUR J IMMUNOL

JF - EUR J IMMUNOL

SN - 0014-2980

IS - 11

ER -