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Rapid expansion of Treg cells protects from collateral colitis following a viral trigger.

Abstract：

:Foxp3+ regulatory T (Treg) cells are essential for maintaining peripheral tolerance and preventing autoimmunity. While genetic factors may predispose for autoimmunity, additional environmental triggers, such as viral infections, are usually required to initiate the onset of disease. Here, we show that viral infection with LCMV results in type I IFN-dependent Treg cell loss that is rapidly compensated by the conversion and expansion of Vβ5+ conventional T cells into iTreg cells. Using Vβ5-deficient mice, we show that these Vβ5+ iTreg cells are dispensable for limiting anti-viral immunity. Rather, the delayed replenishment of Treg cells in Vβ5-deficient mice compromises suppression of microbiota-dependent activation of CD8+ T cells, resulting in colitis. Importantly, recovery from clinical symptoms in IBD patients is marked by expansion of the corresponding Vβ2+ Treg population in humans. Collectively, we provide a link between a viral trigger and an impaired Treg cell compartment resulting in the initiation of immune pathology.

journal_name

Nat Commun

journal_title

Nature communications

authors

Schorer M,Lambert K,Rakebrandt N,Rost F,Kao KC,Yermanos A,Spörri R,Oderbolz J,Raeber ME,Keller CW,Lünemann JD,Rogler G,Boyman O,Oxenius A,Joller N

doi

10.1038/s41467-020-15309-6

subject

Has Abstract

pub_date

2020-03-23 00:00:00

pages

1522

issue

1

issn

2041-1723

pii

10.1038/s41467-020-15309-6

journal_volume

11

pub_type

杂志文章

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