期刊
JCI INSIGHT
卷 5, 期 8, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.135597
关键词
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资金
- IBM Blue Gene Science Program [W1258591, W1464125, W1464164]
- NIH/National Cancer Institute Cancer Center Support Grant [P30 CA008748]
- Pershing Square Sohn Cancer Research grant
- PaineWebber Chair
- Stand Up 2 Cancer
- NIH [R01 CA205426, R35 CA232097, R01CA108835, R21-EB023411, R33-CA229042, P41-EB028239]
- STARR Cancer Consortium
- Precision Immunotherapy Kidney Cancer Fund
- NIH Cancer Nanotechnology Training Center at the Johns Hopkins Institute for NanoBioTechnology
- National Science Foundation Graduate Research Fellowship [DGE-1232825]
- ARCS Foundation
- National Science Foundation Graduate Research Fellowship
- AstraZeneca
- Troper Wojcicki Foundation
Recent studies show gut microbiota modulate antitumor immune responses: one proposed mechanism is cross-reactivity between antigens expressed in commensal bacteria and neoepitopes. We found that T cells targeting an epitope called SVYRYYGL (SVY), expressed in the commensal bacterium Bifidobaderium breve (B. breve), cross-react with a model neoantigen, SIYRYYGL (SIY). Mice lacking B. breve had decreased SVY-reactive T cells compared with B. breve-colonized mice, and the T cell response was transferable by SVY immunization or by cohousing mice without Bifidobactedum with ones colonized with Bifidobacterium. Tumors expressing the model SIY neoantigen also grew faster in mice lacking B. breve compared with Bifidobacteriurn-colonized animals. B. breve colonization also shaped the SVY-reactive TCR repertoire. Finally, SVY-specific T cells recognized SIY-expressing melanomas in vivo and led to decreased tumor growth and extended survival. Our work demonstrates that commensal bacteria can stimulate antitumor immune responses via cross-reactivity and how bacterial antigens affect the T cell landscape.
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