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S1PR1 is crucial for accumulation of regulatory T cells in tumors via STAT3.

Abstract：

:S1PR1 signaling has been shown to restrain the number and function of regulatory T (Treg) cells in the periphery under physiological conditions and in colitis models, but its role in regulating tumor-associated T cells is unknown. Here, we show that S1PR1 signaling in T cells drives Treg accumulation in tumors, limits CD8(+) T cell recruitment and activation, and promotes tumor growth. T-cell-intrinsic S1PR1 affects Treg cells, but not CD8(+) T cells, as demonstrated by adoptive transfer models and transient pharmacological S1PR1 modulation. An increase in S1PR1 in CD4(+) T cells promotes STAT3 activation and JAK/STAT3-dependent Treg tumor migration, whereas STAT3 ablation in T cells diminishes tumor-associated Treg accumulation and tumor growth. Our study demonstrates a stark contrast between the consequences of S1PR1 signaling in Treg cells in the periphery versus tumors.

journal_name

Cell Rep

journal_title

Cell reports

authors

Priceman SJ,Shen S,Wang L,Deng J,Yue C,Kujawski M,Yu H

doi

10.1016/j.celrep.2014.02.016

subject

Has Abstract

pub_date

2014-03-27 00:00:00

pages

992-999

issue

6

issn

2211-1247

pii

S2211-1247(14)00116-8

journal_volume

6

pub_type

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