| Literature DB >> 32907933 |
Maryam Akrami1, Rosemary Menzies1, Kenji Chamoto1, Michio Miyajima2, Ryuji Suzuki3,4, Hiroyuki Sato3, Akiko Nishii5, Michio Tomura5, Sidonia Fagarasan2, Tasuku Honjo6.
Abstract
The gut microbiome has garnered attention as an effective target to boost immunity and improve cancer immunotherapy. We found that B cell-defective (BCD) mice, such as µ-membrane targeted deletion (µMT) and activation-induced cytidine deaminase (AID) knockouts (KOs), have elevated antitumor immunity under specific pathogen-free but not germ-free conditions. Microbial dysbiosis in these BCD mice enriched the type I IFN (IFN) signature in mucosal CD8+ T cells, resulting in up-regulation of the type I IFN-inducible protein stem cell antigen-1 (Sca-1). Among CD8+ T cells, naïve cells predominantly circulate from the gut to the periphery, and those that had migrated from the mesenteric lymph nodes (mLNs) to the periphery had significantly higher expression of Sca-1. The gut-educated Sca-1+ naïve subset is endowed with enhanced mitochondrial activity and antitumor effector potential. The heterogeneity and functional versatility of the systemic naïve CD8+ T cell compartment was revealed by single-cell analysis and functional assays of CD8+ T cell subpopulations. These results indicate one of the potential mechanisms through which microbial dysbiosis regulates antitumor immunity.Entities:
Keywords: IgA; circulation between gut and periphery; gut-microbiota education; mitochondrial activation; type I IFN signaling
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Year: 2020 PMID: 32907933 PMCID: PMC7519229 DOI: 10.1073/pnas.2010981117
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205