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

Michelle Schorer, Katharina Lambert, Nikolas Rakebrandt, Felix Rost, Kung-Chi Kao, Alexander Yermanos, Roman Spörri, Josua Oderbolz, Miro E. Raeber, Christian W. Keller, Jan D. Lünemann, Gerhard Rogler, Onur Boyman, Annette Oxenius and Nicole Joller ()
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Michelle Schorer: University of Zurich
Katharina Lambert: University of Zurich
Nikolas Rakebrandt: University of Zurich
Felix Rost: University of Zurich
Kung-Chi Kao: University of Zurich
Alexander Yermanos: ETH Zurich
Roman Spörri: ETH Zurich
Josua Oderbolz: ETH Zurich
Miro E. Raeber: University Hospital Zurich
Christian W. Keller: University of Zurich
Jan D. Lünemann: University of Zurich
Gerhard Rogler: University Hospital Zurich
Onur Boyman: University Hospital Zurich
Annette Oxenius: ETH Zurich
Nicole Joller: University of Zurich

Nature Communications, 2020, vol. 11, issue 1, 1-13

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-15309-6

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