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      Enhancing cancer immunotherapy with nanomedicine

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      Nature Reviews Immunology

      Springer Science and Business Media LLC

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          Abstract

          Therapeutic targeting of the immune system in cancer is now a clinical reality and marked successes have been achieved, most notably through the use of checkpoint blockade antibodies and chimeric antigen receptor T cell therapy. However, efforts to develop new immunotherapy agents or combination treatments to increase the proportion of patients who benefit have met with challenges of limited efficacy and/or significant toxicities. Nanomedicines — therapeutics composed of or formulated in carrier materials typically less than 100 nm in size — were originally developed to increase the uptake of chemotherapy agents by tumours and to reduce their off-target toxicities. Here, we discuss how nanomedicine-based treatment strategies are well suited to immunotherapy, based on the ability of nanomaterials to direct immunomodulators to tumours and lymphoid organs, to alter the way biologics engage with target immune cells, and to accumulate in myeloid cells in tumours and systemic compartments. We also discuss early efforts towards clinical translation of nanomedicine-based immunotherapy.

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          Most cited references 90

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          Analysis of nanoparticle delivery to tumours

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            Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes.

            Immunological memory in vertebrates is often exclusively attributed to T and B cell function. Recently it was proposed that the enhanced and sustained innate immune responses following initial infectious exposure may also afford protection against reinfection. Testing this concept of "trained immunity," we show that mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner. C. albicans and fungal cell wall β-glucans induced functional reprogramming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the β-glucan receptor dectin-1 and the noncanonical Raf-1 pathway. Monocyte training by β-glucans was associated with stable changes in histone trimethylation at H3K4, which suggests the involvement of epigenetic mechanisms in this phenomenon. The functional reprogramming of monocytes, reminiscent of similar NK cell properties, supports the concept of "trained immunity" and may be employed for the design of improved vaccination strategies. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Mediating tumor targeting efficiency of nanoparticles through design.

              Here we systematically examined the effect of nanoparticle size (10-100 nm) and surface chemistry (i.e., poly(ethylene glycol)) on passive targeting of tumors in vivo. We found that the physical and chemical properties of the nanoparticles influenced their pharmacokinetic behavior, which ultimately determined their tumor accumulation capacity. Interestingly, the permeation of nanoparticles within the tumor is highly dependent on the overall size of the nanoparticle, where larger nanoparticles appear to stay near the vasculature while smaller nanoparticles rapidly diffuse throughout the tumor matrix. Our results provide design parameters for engineering nanoparticles for optimized tumor targeting of contrast agents and therapeutics.
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                Author and article information

                Journal
                Nature Reviews Immunology
                Nat Rev Immunol
                Springer Science and Business Media LLC
                1474-1733
                1474-1741
                January 31 2020
                Article
                10.1038/s41577-019-0269-6
                7536618
                32005979
                © 2020

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