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WIREs Nanomed Nanobiotechnol
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Immunoengineering with biomaterials for enhanced cancer immunotherapy

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Cancer immunotherapy has recently shown dramatic clinical success inducing durable response in patients of a wide variety of malignancies. Further improvement of the clinical outcome with immune related cancer treatment requests more exquisite manipulation of a patient's immune system with increased immunity against diseases while mitigating the toxicities. To meet this challenge, biomaterials applied to immunoengineering are being developed to achieve tissue‐ and/or cell‐specific immunomodulation and thus could potentially enhance both the efficacy and safety of current cancer immunotherapies. Here, we review the recent advancement in the field of immunoengineering using biomaterials and their applications in promoting different modalities of cancer immunotherapies, with focus on cell‐, antibody‐, immunomodulator‐, and gene‐based immune related treatments and their combinations with conventional therapies. Challenges and opportunities are discussed in applying biomaterials engineering strategies in the development of future cancer immunotherapies. This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Oncologic Disease Therapeutic Approaches and Drug Discovery > Emerging Technologies Implantable Materials and Surgical Technologies > Nanomaterials and Implants
Chemically modified oncolytic adenovirus for immuno‐gene therapy. (a) Synthetic scheme of polyethylene glycol (PEG)/lipids/calcium phosphate (CaP)‐OncoAd (PLC‐OncoAd) delivery system for ZD55‐IL‐24, an OncoAd that carries the IL‐24 gene. CaP and ZD55‐IL‐24 were coprecipitated to produce an electron dense biomineral layer. Dioleoylphosphatydic acid (DOPA), an amphiphilic phospholipid, strongly interacted with cations at the interface to stabilize CaP/ZD55‐IL‐24. The mPEG2000–1,2‐dipalmitoyl‐sn‐glycero‐3‐phosphoethanolamine (mPEG‐DPPE) formed a hydrophilic protective layer around the DOPA/CaP/ZD55‐IL‐24 complexes and facilitated long circulation time after intravenous administration. (b) Fluorescence images of excised tumors and organs 4 days after the intravenous injection of ZD55‐GFP or PLC‐ZD55‐GFP for the delivery of GFP as a model gene in nude mice bearing Huh‐7 xenograft. GFP: green fluorescence protein. (c) Tumor growth curves of subcutaneous Huh‐7 tumors in nude mice injected with PLC‐OncoAd encoding IL‐24 (PLC‐ ZD55‐IL‐24). LD: low dose = 7.5 × 109 viral particles (VPs); HD: high dose = 1.5 × 1010 VPs. (Reprinted with permission from Chen et al. (). Copyright 2016 American Chemical Society)
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Lymph node‐focused delivery of small‐molecule Toll‐like receptor (TLR) agonist for cancer immunotherapy. (a) Schematic overview and corresponding chemical structures of degradable immune‐stimulatory nanogels. (i) Block copolymers self‐assemble in dimethyl sulfoxide (DMSO) into NPs; (ii) Covalent ligation of 1‐(4‐(aminomethyl)benzyl)‐2‐butyl‐1H‐imidazo[4,5‐c]quinolin‐4‐amine (IMDQ), a TLR7/8 agonist (green) and cross‐linking. (iii) Conversion of residual pentafluorophenyl ester with 2‐ethanolamine yielding fully hydrated nanogels after transferring to the aqueous phase. (b, c) In vivo bioluminescence in interferon‐β reporter mice. Images recorded at 4, 8, and 24 h following injection of soluble IMDQ (b) and nanogel‐ligated IMDQ (c) in the footpad (each at 10‐μg IMDQ equivalents). DLN: draining lymph node. (Reprinted with permission from Nuhn et al. (). Copyright 2016 National Academy of Sciences, USA)
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Microneedle patch for enhanced efficacy of checkpoint blockade antibody therapy. (a) Schematic view of the anti‐PD‐1 antibody (aPD1) delivered by a microneedle (MN) patch loaded with physiologically self‐dissociated NPs. With glucose oxidase/catalas (GOx/CAT) enzymatic system immobilized inside the NPs by double‐emulsion method, the enzyme‐mediated conversion of blood glucose to gluconic acid promoted the sustained dissociation of NPs, subsequently leading to the release of aPD1. (b) Mouse dorsum and relevant skin (the area within the red dashed line) was transcutaneously treated with a MN patch (left), with the image of the trypan blue staining showing the penetration of MN patch into the mouse skin (right) (scale bar, 1 mm). (c) Merged fluorescence and bright field image of the mouse skin penetrated by MNs loaded with fluorescein isothiocyanate (FITC)‐labeled aPD1 (shown in green) (scale bar, 200 μm). (d) Quantified bioluminescence signal of the subcutaneously implanted B16‐F10 tumors in mice treated with MN patch (with GOx), free aPD1, or aPD1‐loaded MN patch with or without GOx through a single local administration at the tumor site. (e) Kaplan–Meier survival curves for the treated and untreated mice. (Reprinted with permission from Wang et al. (). Copyright 2016 American Chemical Society)
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Hijacking immune cells for drug delivery. (a) Schematic view of T‐cell functionalization and cell‐mediated delivery of topoisomerase I poison SN‐38 nanocapsules (NCs) into tumors. (Reprinted with permission from Huang et al. (). Copyright 2015 American Association for the Advancement of Science) (b) Schematic illustration of the delivery of anti‐PD‐L1 antibody (aPDL1) to the primary‐tumor resection site by platelets. MHC, major histocompatibility complex; PMPs, platelet‐derived microparticles; P‐aPDL1, aPDL1‐conjugated platelets. (c) Confocal immunofluorescence images of B16 cancer cells co‐incubated with nonactivated (left) and activated (right) P‐aPDL1 in a transwell system (pore size: 1 μm). P‐aPDL1 and B16 cancer cells were cultured in upper and lower compartments, respectively. Red, blue and green fluorescence indicates aPDL1, nucleus and plasma membrane, respectively. Scale bar, 20 μm. (d, e) Recurrent tumor growth (d) and survival curves (e) of mice bearing a mouse melanoma model with incomplete‐tumor‐resection. B16‐F10 tumors were surgically resected in part followed by i.v. injection of phosphate‐buffered saline (PBS), platelets, aPDL1 or P‐aPDL1 (dose of aPDL1, 1 mg kg−1). (Reprinted with permission from Wang et al. (). Copyright 2017 Nature Publishing Group)
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In vivo programming of circulating T‐cells into antigen‐specific T‐cells by synthetic DNA NPs. (a) Design and manufacture of lymphocyte‐programming DNA NPs. The plasmid DNA encoded the leukemia‐specific 194‐1BBz chimeric antigen receptor (CAR) and the hyperactive iPB7 transposase was mixed with poly(β‐amino ester) (PBAE) polymer functionalized with microtubule‐associated‐nuclear localization (MTAS‐NLS) peptides to form the DNA NPs. The surfaces of PBAE NPs was then coupled with T‐cell‐targeting anti‐CD3e f(ab′)2 fragments, which selectively enabled CD3‐mediated endocytosis by T‐cells. (b) CAR+ peripheral T‐cells frequency following the injection of NPs delivering DNA that encoded leukemia‐specific 194‐1BBz with iPB7, tumor‐irrelevant P4‐1BBz CAR genes, or 194‐1BBz transgene alone. (c) NPs‐programmed CAR‐T cells induced tumor regression and increased overall survival similarly as adoptively transferred T‐cells transduced ex vivo. (Reprinted with permission from Smith et al. (). Copyright 2017 Nature Publishing Group)
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Schematic view of examples of immunoengineering strategies for enhancing different modalities of cancer immunotherapies. CTL, cytotoxic T lymphocyte; CAR, chimeric antigen receptor; TCR, T‐cell receptor; aAPC, artificial antigen‐presenting cell; NPs, nanoparticles; PD‐1, programmed cell death protein 1; CTLA‐4, cytotoxic T‐lymphocyte‐associated protein 4; siRNA, small interfering RNA; DC, dendritic cell; TLR, Toll‐like receptor; mAb, monoclonal antibody
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Immunotherapy in combination with photothermal therapy (PTT). (a) The mechanism of anti‐tumor immune responses induced by a NP‐based PTT in combination with anti‐cytotoxic T‐lymphocyte antigen‐4 (CTLA‐4) checkpoint‐blockade. Indocyanine green (ICG), a photothermal agent, and imiquimod (R837), a Toll‐like‐receptor‐7 agonist, were co‐encapsulated by poly(lactic‐co‐glycolic) acid (PLGA) to form the NP for PTT. Th, helper T lymphocyte; NK, natural killer cell; Treg, regulatory T‐cell; mAb, monoclonal antibody. (b) Secondary tumor growth curves of different groups of mice with subcutaneous 4T1 tumors after various treatments to eliminate their primary tumors. (c) Morbidity‐free survival of different groups of mice with metastatic 4T1 tumors after various treatments indicated to eliminate their primary tumors (the numbers labeling the curves indicate the corresponding treatments in (b)). (Reprinted with permission from Chen et al. (). Copyright 2016 Nature Publishing Group)
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