Cover ImageThe oral microbiome plays a role in shaping antitumor immunity. Porphyromonas gingivalis (P. gingivalis) is an oral anaerobic bacterium known for inducing microbiome dysbiosis and chemotherapy resistance. Ren, Han et al. reveal the immune-suppressive function of P. gingivalis and demonstrate the bacterium's effects that facilitate the progression of oral cancer. Mechanistically, P. gingivalis infection induces upregulation of PD-L1 on dendritic cells via activation of Akt/STAT, which then are able to suppress antitumor functions of CD8+ T cells. The data highlight potential targets for improving the efficacy of immunotherapy in oral cancer.Read more in this issue on page 290. Original image from Fig. 7I. Artwork by Lewis Long.Close Modal
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Cancer Immunology Research (2013-Present)(ISSN 2326-6066) Published monthly since 2013.
Cancer Immunity (2001-2013; volumes 1-13)(EISSN 1424-9634) Published periodically from 2001-2013.
Table of Contents
What We're Reading
Syntaphilin Regulates Neutrophil Migration in Cancer
The authors identify syntaphilin as a regulator of spontaneous migration of neutrophils in cancer. Syntaphilin deletion promotes PMN spontaneous migration and metastasis via increased mitochondria motility, elevated rates of oxidative phosphorylation and glycolysis, and increased generation of adenosine.
P. gingivalis Infection Upregulates PD-L1 Expression on Dendritic Cells, Suppresses CD8+ T-cell Responses, and Aggravates Oral Cancer
Immunosuppressive properties of the oral anaerobic bacterium Porphyromonas gingivalis are revealed, highlighting effects of the bacterium that facilitate oral cancer progression. The data suggest that P. gingivalis, and/or signaling it mediates, can be targeted to improve immunotherapy efficacy.
CD161 Characterizes an Inflamed Subset of Cytotoxic T Lymphocytes Associated with Prolonged Survival in Human Papillomavirus–Driven Oropharyngeal Cancer
CD161 characterizes an inflamed subset of cytotoxic T lymphocytes that have high expression of immune checkpoints while retaining high cytotoxic capability. These cells can be reinvigorated by immune checkpoint blockade and are a biomarker for clinical benefit.
CD8+ T cell–Dependent Remodeling of the Tumor Microenvironment Overcomes Chemoresistance
The authors find that CD161 is overexpressed on a subset of CD8+ T cells in chemoresistant breast tumors and drives T-cell dysfunction. CD161 provides a potential target to enhance antitumor immunity and reverse chemoresistance.
PHD2 Constrains Antitumor CD8+ T-cell Activity
How hypoxia-sensing proteins regulate antitumor immunity is incompletely understood. The authors show stabilization of HIF-1α promotes recruitment, survival and/or differentiation of polyfunctional CD8+ T cells into the tumor and synergizes with PD-1 blockade to control tumor growth.
Infiltration of Tumors Is Regulated by T cell–Intrinsic Nitric Oxide Synthesis
Loss of nitric oxide synthase is shown to debilitate cytotoxic T cells in the therapeutic setting. Although nitric oxide is typically characterized as immunosuppressive, these data highlight its key intrinsic role in modulating T-cell tumor infiltration and suppression.
Tumor-Associated CD19+CD39− B Regulatory Cells Deregulate Class-Switch Recombination to Suppress Antibody Responses
The authors identify an IL10-producing CD19+CD39− immunoregulatory B-cell subset (Breg cells) in breast cancer patients. The Breg cells inhibit H-chain class-switch recombination and generation of antibody-producing B cells by limiting autologous Tfh-cell differentiation and IL21 production.
Cancer Cell Resistance to IFNγ Can Occur via Enhanced Double-Strand Break Repair Pathway Activity
Cancer cells can become resistant to the antitumor effects of IFNγ. Using high-throughput transcriptomic profiling and CRISPR screens, the authors demonstrate a relationship between the DSB repair pathway and IFNγ resistance, suggesting a potential new combination treatment strategy.