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CTLA-4-expressing ILC3s restrain interleukin-23-mediated inflammation

Subsets of ILC3s upregulate the immunoregulatory checkpoint molecule CTLA-4 after stimulation in a microbiota-dependent manner, and advances to support CTLA-4⁺ ILC3s may represent a treatment opportunity in IL-23-driven chronic inflammation.

Anees Ahmed
Ann M. Joseph
Gregory F. Sonnenberg
Research12 Jun 2024
Nature

Volume: 630, P: 976-983
ILC3s select microbiota-specific regulatory T cells to establish tolerance in the gut

ILC3s expressing MHC class II control the fate of inflammatory versus tolerogenic T cells that respond to the microbiota by selecting for antigen-specific RORγt⁺ T_reg cells and against T_H17 cells, establishing intestinal homoeostasis.

Mengze Lyu
Hiroaki Suzuki
Gregory F. Sonnenberg
Research07 Sept 2022
Nature

Volume: 610, P: 744-751
Innate lymphoid cells support regulatory T cells in the intestine through interleukin-2

A microbiota- and IL-1β-dependent axis of IL-2 production by group-3 innate lymphoid cells is shown in a mouse model to be necessary to maintain immunological homeostasis and regulatory T cells in the small intestine.

Lei Zhou
Coco Chu
Gregory F. Sonnenberg
Research03 Apr 2019
Nature

Volume: 568, P: 405-409
Regulatory T cells infiltrate the tumor-induced tertiary lymphoïd structures and are associated with poor clinical outcome in NSCLC

Regulatory T cells (Tregs) have similar immune profiles in tertiary lymphoid structures of lung cancer and non-TLS areas, with tumor-infiltrating Tregs found to inhibit the proliferation and cytokine secretion of CD4 + conventional T cells.

Priyanka Devi-Marulkar
Solène Fastenackels
Marie-Caroline Dieu-Nosjean
ResearchOpen Access24 Dec 2022
Communications Biology

Volume: 5, P: 1-16

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CTLA-4-expressing ILC3s restrain interleukin-23-mediated inflammation

ILC3s select microbiota-specific regulatory T cells to establish tolerance in the gut

Innate lymphoid cells support regulatory T cells in the intestine through interleukin-2

Regulatory T cells infiltrate the tumor-induced tertiary lymphoïd structures and are associated with poor clinical outcome in NSCLC

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