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Difference in Th1 and Th17 Lymphocyte Adhesion to Endothelium
Author(s) -
Alcaide Pilar,
MagantoGarcia Elena,
Newton Gail,
Travers Richard,
Croce Kevin,
Bu DeXiu,
Luscinskas Francis W,
Lichtman Andrew H
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.38.1
Subject(s) - microbiology and biotechnology , endothelium , cell adhesion , cell adhesion molecule , adhesion , ccl20 , flow cytometry , chemistry , inflammation , soluble cell adhesion molecules , icam 1 , immunology , biology , chemokine , chemokine receptor , endocrinology , organic chemistry
T cell subset specific migration to inflammatory sites is tightly regulated and involves interaction of the T cells with the endothelium. T helper 17 (Th17) cells often appear at different inflammatory sites than T helper 1 (Th1) cells, or both subsets appear at the same sites, but at different times. Differences in T cell subset adhesion to endothelium may contribute to subset‐specific migratory behavior, but this possibility has not been well studied. We examined the adhesion of Th17 cells to endothelial adhesion molecules and endothelium under flow in vitro and in vivo, and characterized their migratory phenotype by flow cytometry and qRT‐PCR. More Th17 than Th1 cells interacted with E‐selectin, and Th17 adhesion to ICAM‐1 was dependent on integrin activation by CCL20. Fewer Th17 than Th1 cells bound to TNF‐activated E‐selectin deficient endothelial cells. Intravital microscopy demonstrated that Th17 cells engage in more rolling interactions with TNF‐α treated cremaster microvessels than Th1 cells. Both in vitro and in vivo generated Th17 cells efficiently migrated to the inflamed peritoneal cavity. These data provide evidence that interactions of Th17 and Th1 cells with endothelium are quantitatively different and open a window to develop T cell subset‐specific therapeutic interventions based in their distinct migratory phenotypes. Funded by NIH K99/R00 HL94706‐02 and HL36028.