ArticleThe Journal of experimental medicine2026
B7 costimulation antagonizes RORγt+ regulatory T cells and immune tolerance in the intestine.
Article in The Journal of experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Regulatory T (Treg) cells that recognize dietary- or microbiota-derived antigens express RORγt and are essential for immune tolerance in the intestine. A recent paradigm shift found these cells require major histocompatibility complex class II (MHCII) on RORγt+ antigen-presenting cells (APCs) rather than conventional dendritic cells (cDCs) for signal one. Here, we evaluate signal two and unexpectedly find that costimulatory molecules B7-1 (CD80) and B7-2 (CD86) antagonize the generation of microbiota-specific RORγt+ Treg cells. Gain-of-function or loss-of-function therapeutics targeting B7 via CTLA-4 exert reciprocal effects on the generation of microbiota-specific RORγt+ Treg cells. This axis was independent of B7 on RORγt+ APCs but required MHCII on this cell type. Finally, CTLA4-Ig treatment restores microbiota-specific RORγt+ Treg cell generation and protects from experimental intestinal inflammation induced by pathobiont colonization with IL-10R signaling blockade. These results define that RORγt+ Treg cells are uniquely restrained by B7 costimulation, while CTLA4-Ig enhances immune tolerance in the intestine when acting cooperatively with RORγt+ APCs.
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