Regulatory T cells suppress GM-CSF-producing T helper cells via IL-2 modulation to restrain immunopathology

Summary: Regulatory T (Treg) cells are critical for maintaining peripheral tolerance and preventing autoimmunity. Treg cell depletion or dysfunction results in fatal multiorgan inflammation linked to unrestrained effector T cell expansion. Here, we combine in vivo gene targeting and fate-mapping wit...

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Main Authors: Sara Costa-Pereira, Margit Lanzinger, Nicolás Núñez, Juan Villar-Vesga, Myrto Andreadou, Francesco Prisco, Philipp Häne, Elsa Roussel, Sinduya Krishnarajah, Rachel Chanel Lindemann, Laura Oberbichler, Frederike Westermann, André Fonseca Da Silva, Virginia Cecconi, Mirjam Pinzger, Sonia Tugues, Sarah Mundt, Melanie Greter, Donatella De Feo, Burkhard Becher
Format: Article
Language:English
Published: Elsevier 2025-05-01
Series:Cell Reports
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Online Access:http://www.sciencedirect.com/science/article/pii/S2211124725004139
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Summary:Summary: Regulatory T (Treg) cells are critical for maintaining peripheral tolerance and preventing autoimmunity. Treg cell depletion or dysfunction results in fatal multiorgan inflammation linked to unrestrained effector T cell expansion. Here, we combine in vivo gene targeting and fate-mapping with high-dimensional cytometry to identify Treg cells’ steady-state function and suppressive mechanisms that prevent autoimmune inflammation and dissect the T helper (TH) cell-derived cytokines and responding cells executing tissue damage upon global loss of peripheral tolerance. We unveil that type 1 cytokines, granulocyte-macrophage colony-stimulating factor (GM-CSF) and interferon (IFN)γ, but not interleukin (IL)-17A, direct the ensuing immunopathology and mortality. GM-CSF orchestrates tissue invasion by monocytes and granulocytes and enhances their reactive oxygen species production and phagocytic capability. IL-2 modulation by Treg cells is crucial in restraining pathogenic GM-CSF-producing TH cells. Our study highlights the critical role of Treg cells and IL-2 signaling in controlling GM-CSF-producing TH cells and type 1 responses to curb phagocyte-mediated tissue destruction.
ISSN:2211-1247