Polyclonal Treg cells modulate T effector cell trafficking.

Polyclonal Treg cells modulate T effector cell trafficking.
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DOI:
10.1002/eji.201141503
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发表时间:
2011-10
影响因子:
5.4
通讯作者:
Shevach, Ethan M.
Shevach, Ethan M.
中科院分区:
医学3区
文献类型:
--
作者:
Davidson, Todd S.;Shevach, Ethan M.

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In this study, we have analyzed the in vivo dynamics of the interaction between polyclonal Foxp3+ Tregs, effector T (Teff) cells, and DCs in order to further our understanding of the mechanisms of Treg-mediated suppression. Co-transfer of polyclonal activated Tregs into normal mice attenuated the induction of EAE. Suppression of disease strongly correlated with a reduced number of Teff cells in the spinal cord, but not with Treg-mediated inhibition of Th1/Th17 differentiation. Co-transfer of Tregs with TCR Tg Teff cells followed by immunization by multiple routes resulted in an enhanced number of Teff cells in the lymph nodes draining the site of immunization without an inhibition of Teff cell differentiation. Fewer Teff cells could be detected in the blood in the presence of Tregs and fewer T cells could access a site of antigen exposure in a modified delayed type hypersensitivity assay. Teff cells recovered from LN in the presence of Tregs expressed decreased levels of CXCR4, syndecan, and the sphingosine phosphate receptor, S1P1. Thus, polyclonal Tregs influence Teff cell responses by targeting trafficking pathways, thus allowing immunity to develop in lymphoid organs, but limiting the number of potentially auto-aggressive cells that are allowed to enter the tissues.
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