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Regulatory T cells dynamically regulate selectin ligand function during multiple challenge contact hypersensitivity (146.12)
Author(s) -
Hickey Michael,
Abeynaike Latasha,
Deane James,
Westhorpe Clare,
Issekutz Andrew
Publication year - 2014
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.28.1_supplement.146.12
Subject(s) - foxp3 , inflammation , microbiology and biotechnology , population , immunology , chemistry , in vitro , regulatory t cell , t cell , biology , il 2 receptor , medicine , immune system , biochemistry , environmental health
Regulatory T cells (Tregs) play critical roles in regulation of T cell‐mediated inflammation, and in organs such as the skin, this is dependent on their expression of selectin ligands required for rolling in peripheral microvessels. However, whether there are differences in the molecules used by Tregs and pro‐inflammatory T cells to undergo rolling remains unclear. Here we used spinning disk confocal microscopy of Foxp3‐GFP mice to visualize rolling of endogenous Tregs in dermal postcapillary venules. Tregs were observed to undergo infrequent but consistent rolling interactions under resting and inflamed conditions. Despite this, during inflammation, Tregs were able to adhere efficiently, comprising 40% of the total adherent CD4 + T cell population at the peak of the response. In a multiple challenge model of contact sensitivity, rolling of both Tregs and conventional CD4 + T cells was mostly dependent on overlapping contributions of P‐ and E‐selectin. However, shortly after a second challenge, rolling of Tregs but not conventional T cells became P‐selectin‐independent, an effect associated with a reduction in their capacity to bind P‐selectin in vitro . These findings demonstrate that Treg selectin‐binding capacity and the molecular basis of Treg rolling in the peripheral microvasculature can be regulated dynamically in a multiple challenge model of inflammation.