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TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling

by Zidi, Bochra , N’guessan, Prudence , Seillier, Marion , Vandevelde, Amelle , Poplineau, Mathilde , Pouyet, Laurent , Vincent-Fabert, Christelle , Mancini, Stéphane , Carrier, Alice , Guittard, Geoffrey , Duprez, Estelle

in Life Sciences

2018

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TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling

in Life Sciences

2018

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Journal Article

TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling

Zidi, Bochra,

N’guessan, Prudence,

Seillier, Marion,

Vandevelde, Amelle,

Poplineau, Mathilde,

Pouyet, Laurent,

Vincent-Fabert, Christelle,

Mancini, Stéphane,

Carrier, Alice,

Guittard, Geoffrey,

Duprez, Estelle

2018

Overview

Significance Reactive oxygen species (ROS) play a role in signaling in immune cells, in particular in B cell activation and terminal differentiation in secondary lymphoid organs. Nevertheless, their role in B cell development in the bone marrow (BM) still remains poorly explored. TP53INP1 is a target of the tumor suppressor p53, which mediates its antioxidant activity. We report the surprising observation that chronic oxidative stress in TP53INP1-deficient mice rescues B lymphopoiesis in the BM during aging. ROS sustain IL-7R signaling in aged TP53INP1-deficient BM through maintenance of active STAT5 transcription factor, driving the expression of the B lineage Pax5 transcription factor. This work suggests that antioxidants cannot be in favor of antibody-producing cell development.

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Publisher

National Academy of Sciences

Subject

Life Sciences