Jared H. Rowe

Boston Children's Hospital

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Arlene H. Sharpe

Boston VA Research Institute

Marcia C. Haigis

Harvard University

Gordon J. Freeman

Dana-Farber Cancer Institute

Shakchhi Joshi

Harvard University

Megan E. Fung

Harvard University

Joon Seok Park

Samsung (South Korea)

Sheila Johnson

Harvard University

Ilaria Elia

KU Leuven

Kristen E. Pauken

Harvard University

Osmaan Shahid

Boston VA Research Institute

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Harvard University

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Boston Children's Hospital

Dana-Farber Cancer Institute

Brigham and Women's Hospital

Boston Children's Museum

Massachusetts General Hospital

Boston VA Research Institute

Dana-Farber/Boston Children's Cancer and Blood Disorders Center

Broad Institute

Massachusetts Institute of Technology

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Supplementary Figure 1 from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

Supplementary Figure 1 shows the approach for rapid magnetic bead based separation of OT-1 cells and peptide pulsed splenocytes for metabolomic analysis.

Splenocyte

10.1158/2159-8290.24792919

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Supplementary Figure 2 from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

Supplementary Figure 2 shows the one carbon enzyme expression levels and serine biosynthesis following activation of CD8+ T cells with varying concentrations of anti-CD3.

10.1158/2159-8290.24792895.v1

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Supplementary Figure 3 from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

Supplementary Figure 3 shows the cytotoxicity of previously activated CD8+ T cells with or without the SHMT inhibitor.

10.1158/2159-8290.24792892.v1

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Supplementary Figure 15 from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

Supplementary Figure 15 shows the effects of formate treatment on TCF1 and TIM3 expression in tumor infiltrating "bystander cells."

Bystander effect

10.1158/2159-8290.24792898.v1

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Immune suppressive molecules and regulatory T cells control host defense against Listeria monocytogenes infection

Jared H. Rowe

University of Minnesota Ph.D. dissertation. June 2012. Major: Microbiology, Immunology and Cancer Biology. Advisor: Sing Sing Way M.D. Ph.D. 1 computer file (PDF); xi, 234 pages.

Host response

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Figure S2 from Age-Associated Contraction of Tumor-Specific T Cells Impairs Antitumor Immunity

Peter Georgiev SeongJun Han Amy Y. Huang Thao H. Nguyen Jefte M. Drijvers

Supplemental Figure 2

10.1158/2326-6066.27602081

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Data from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

<div>AbstractThe tumor microenvironment (TME) restricts antitumor CD8+ T-cell function and immunotherapy responses. Cancer cells compromise the metabolic fitness of CD8+ T cells within the TME, but the mechanisms are largely unknown. Here we demonstrate that one-carbon (1C) metabolism is enhanced in T cells in an antigen-specific manner. Therapeutic supplementation of 1C metabolism using formate enhances CD8+ T-cell fitness and antitumor efficacy of PD-1 blockade in B16-OVA tumors. Formate supplementation drives transcriptional alterations in CD8+ T-cell metabolism and increases gene signatures for cellular proliferation and activation. Combined formate and anti–PD-1 therapy increases tumor-infiltrating CD8+ T cells, which are essential for enhanced tumor control. Our data demonstrate that formate provides metabolic support to CD8+ T cells reinvigorated by anti–PD-1 to overcome a metabolic vulnerability in 1C metabolism in the TME to further improve T-cell function.Significance:This study identifies that deficiencies in 1C metabolism limit the efficacy of PD-1 blockade in B16-OVA tumors. Supplementing 1C metabolism with formate during anti–PD-1 therapy enhances CD8+ T-cell fitness in the TME and CD8+ T-cell–mediated tumor clearance. These findings demonstrate that formate supplementation can enhance exhausted CD8+ T-cell function.<a href="https://aacrjournals.org/cancerdiscovery/article/doi/10.1158/2159-8290.CD-23-1059" target="_blank">See related commentary by Lin et al., p. 2507.</a><a href="https://aacrjournals.org/cancerdiscovery/article/doi/10.1158/2159-8290.CD-13-12-ITI" target="_blank">This article is featured in Selected Articles from This Issue, p. 2489</a></div>

10.1158/2159-8290.c.6976555.v1

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Supplementary Figure 5 from Formate Supplementation Enhances Antitumor CD8+ T-cell Fitness and Efficacy of PD-1 Blockade

Jared H. Rowe Ilaria Elia Osmaan Shahid Emily F. Gaudiano Natalia E. Sifnugel

Supplementary Figure 5 shows Chimeric IMmune Editing (CHIME) can disrupt Phgdh causing loss of PHGDH expression and serine biosynthesis in CD8+ T cells.

10.1158/2159-8290.24792886.v1

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Early eradication of persistent Salmonella infection primes antibody-mediated protective immunity to recurrent infection

Microbes and Infection (2010)

Tanner M. Johanns Calvin Law Lokeshchandra Kalekar Hope O’Donnell James M. Ertelt

Salmonella infection

Adoptive Cell Transfer

10.1016/j.micinf.2010.11.004

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Regulatory T cell suppressive potency dictates the balance between bacterial proliferation and clearance during persistent Salmonella infection (137.11)

The Journal of Immunology (2010)

Tanner M. Johanns James M. Ertelt Jared H. Rowe Joseph C. Lai Sing Sing Way

Abstract The pathogenesis of persistent infection is dictated by the balance between opposing immune activation and suppression signals. Although regulatory T cells (Tregs) have been widely implicated to control host defense against infection, their role in dictating the natural progression of persistent infection remains incompletely defined. Herein, a sharp dichotomy in infection tempo between early and late time points during persistent Salmonella infection is demonstrated. Early after infection, blunted effector T cell activation and increasing bacterial burden coincide with enhanced Treg suppressive potency. Reciprocally, at later time points, robust effector T cell activation and bacterial clearance occur in parallel with diminished Treg suppression. By enumerating the relative impact of Treg ablation on infection outcome at both early and late time points of persistent infection, the role of Treg suppressive potency in dictating the natural progression of infection was verified. Thus, dynamic control of Treg suppressive potency dictates the tempo of persistent bacterial infection.

Salmonella infection

Pathogenesis

10.4049/jimmunol.184.supp.137.11

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