We are analyzing https://link.springer.com/article/10.1186/s40425-016-0110-8.

Title:
Toll-like receptor agonist therapy can profoundly augment the antitumor activity of adoptively transferred CD8+ T cells without host preconditioning | Journal for ImmunoTherapy of Cancer
Description:
Background Lymphodepletion enhances adoptive T cell transfer (ACT) therapy by activating the innate immune system via microbes released from the radiation-injured gut. Microbial components, such as LPS, are key mediators of total body irradiation (TBI) enhancement, but our ability to strategically use these toll-like receptor (TLR) agonists to bolster the potency of T cell-based therapies for cancer remains elusive. Herein, we used TLR4 agonist LPS as a tool to address how and when to use TLR agonists to effectively improve cancer immunotherapy. Methods To determine the mechanisms of how innate immune activation via lymphodepletion potentiated antitumor T cell immunity, we utilized the pmel-1 melanoma mouse model. B16F10-bearing mice were preconditioned with 5Gy TBI and given a tripartite ACT therapy (consisting of transferred pmel-1 CD8+ T cells, vaccination with fowlpox encoding gp100, and IL-2) along with TLR4 agonist LPS. The timing of LPS administration and the requirement of individual components of the tripartite therapy were evaluated based on tumor growth and the phenotype of recovered splenocytes by flow cytometry. We also evaluated the role of non-toxic and clinically used TLR4 and TLR9 agonists—monophosphoryl lipid A (MPL) and CpG Oligodeoxynucleotide (CpG ODN), respectively— for ACT therapy. Results Here we report that while exogenous administration of LPS was able to enhance adoptively transferred CD8+ T cells’ tumor destruction, LPS treatment alone did not replace individual components of the tripartite ACT regimen, or obviate TBI. Moreover, we found that sequentially administering LPS during or one day prior to ACT therapy compromised tumor regression. In contrast, administering LPS after ACT potentiated the antitumor effectiveness of the regimen, thereby supporting the expansion of transferred tumor-specific CD8+ T cells over host CD4+ T cells. We also found that non-toxic TLR agonists MPL and CpG potentiated the antitumor activity of infused CD8+ T cells. Finally, TBI was no longer needed to regress tumors in mice who were depleted of host CD4+ T cells, given a tripartite ACT regimen and then treated with low dose LPS. Conclusions Collectively, our results identify how and when to administer TLR agonists to augment T cell-based immunotherapy in the absence or presence of host preconditioning for treatment of advanced malignancies. Our findings have clinical implications for the design of next generation immune-based therapies for patients with cancer.
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Keywords {🔍}

cells, lps, mice, act, pubmed, article, tbi, treatment, pmel, irradiated, google, scholar, tlr, host, fig, cas, tumor, pfi, data, therapy, day, cancer, cell, antitumor, transferred, immune, nonirradiated, regimen, immunotherapy, infused, central, innate, tripartite, vaccination, days, adoptive, animals, shown, transfer, melanoma, received, lymphodepletion, agonists, found, dcs, agonist, enhances, untreated, experiments, fowlpox,

Topics {✒️}

mage-a3/poly-iclc immunizations acute graft-versus-host disease human papillomavirus-targeted tumor-infiltrating bacterial-derived agonist cpg-dna article download pdf commensal host-microbe relationship cell-based tumor immunity small-cell lung cancer cell-mediated tumor eradication activated cd11b+cd11chicd86hi dcs myeloid-derived suppressor cells fitc-conjugated anti-brdu cell-mediated tumor regression cell-mediated tumor immunotherapy adoptive t-cell transfer chimeric antigen receptor-modified commensal host-microbial relationships unpaired t-test myd88–/– tumor-bearing mice poorly immunogenic melanoma infused tumor-specific cd8+ single cell suspensions receptor 4-dependent contribution transferred tumor-specific cd8+ full access generation immune-based therapies mary jo turk pfi + lps + anti-cd4 acute lymphoid leukemia b16f10-bearing mice tlr9 agonists—monophosphoryl lipid negatively-isolated pmel cd8+ myd88-dependent signaling privacy choices/manage cookies 5gy cpg post-pfi fowlpox encoding gp100 ultra-pure lps porter dl 5gy pfi post-lps tumor-reactive lymphocytes objective response rate concomitant tumor immunity related subjects fowlpox expressing hpg100 5gy pfi pre-lps promote tumor regression extramural research program tumor-infiltrating lymphocytes cell-based immunotherapy creative commons license

Questions {❓}

Though the LPS signal is meant to enhance the donor CD8+ T cells, particularly in the case of administering LPS before T cell infusion, it appears that this beneficial signal bolsters the generation of host immune cells over tumor specific T cells (Is this a phenomenon restricted to ACT therapy or does it impair vaccines, chemotherapy and/or checkpoint modulators as well?

Schema {🗺️}

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            Innate immunity
            Oncology
            Immunology
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         Total body Irradiation
         Adoptive immunotherapy
         CD8+ T lymphocytes
         Innate immunity
         Oncology
         Immunology
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      name:Microbiology and Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, USA
      name:Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, USA
      name:Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, USA
      name:Microbiology and Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, USA
      name:Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, USA
      name:Microbiology and Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, USA

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