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as APCs to boost T cell immunity [93]. Iron-dextran NPs were modified with MHC-I
and CD28 antibodies on their surface to bind to both T cell receptors and CD28 [93].
Magnetic fields drove the cluster aggregation of T cells by the antigen-presenting NPs,
thereby proliferating T cells and expanding the population of antigen-specific CD8
T cells [93]. The administration of T cells followed by signal clustering of T cells dramatically reduced tumor volume and improved survival by generating antigen-specific
+
CD8
T cells in spleen and lymph nodes [93].
DC-tumor fusion cell membranes were developed to mimic copresentation of tumor
antigens and costimulatory molecules by mature DCs [94]. The administration of
DC-tumor fusion NPs significantly expanded the population of CD4
+
and CD8
T cells in the spleen and enabled high secretion of IFN-γ [94]. The vaccination of
DC-tumor fusion NPs prevented the establishment of the tumor, resulting from a considerable increase in the population of tetramer
+
CD8+T cells [94]. Additionally, treatment of DC-tumor fusion NPs in tumor-bearing mouse model highly suppressed tumor
proliferation by recruiting tetramer
+
CD8+T cells and producing IFN-γ [94].
The blockade of immune checkpoints is capable of antagonizing T cell immunity to
sensitize tumor immune surveillance [88,95]. Recently, the development of immune
checkpoint inhibitors harmonized with nanotechnology has been shown to enhance
therapeutic index by adding several critical characteristics such as extended pharmacokinetic, specificity to the tumor, and efficient blockade of immune checkpoints [19,96,97].
For one example, PD-L1 antibody-labeled platelets ameliorated antitumor immunity for
post-surgical cancer immunotherapy [96]. Inspired by the intrinsic properties of platelets,
PD-L1 antibodies were conjugated to the surface of platelets to prevent post-surgical
tumor recurrence [96]. With the aid of platelets, PD-L1 receptors overexpressed on cancer cells after surgery were efficiently blocked by the PD-L1 antibodies from PD-L1
antibody-platelets [96]. The non-activated platelets were so stable that the long systemic
circulation could be induced while PD-L1 antibodies were rapidly released at surgical
sites by activating the platelets [96]. Tumor recurrence of PD-L1 antibody-platelets
was nearly abolished compared to monotreatment of PD-L1 antibody. Additionally,
PD-L1 antibody-platelets significantly triggered a robust, T cell-mediated antitumor
immunity by infiltrating cytotoxic CD4
+
and CD8+T cells into the tumor tissues
[96]. Moreover, the establishment of robust and systemic antitumor immunity by
PD-L1 antibody-platelets completely inhibited lung metastasis [96]. Likewise in a different study, NPs with PD-L1 antibodies substantially increased the antagonist effect of
immune checkpoint blockade to improve antitumor immunity [97].
Poly(amidoamine) dendrimers were tethered with PD-L1 antibodies to induce multivalent binding of the NPs to PD-L1 receptor overexpressed on cancer cells Binding of the
PD-L1 antibody-NPs to PD-L1 receptors could be saturated at lower dosage compared
to PD-L1 antibody treatment [97]. After blocking the PD-L1 receptors on cancer cells,
the treatment of DOX ameliorated the cytotoxic effect to cancers compared with
227Challenges and opportunities of nanotechnology in cancer immunotherapy
+
+
228 DaeYong Lee et al.
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monotreatment of DOX [97]. Dual inhibition of immune checkpoint inhibitors modulated immunosuppressive environments by blocking CTLA-4 and PD-L1 to synergistically elicit enhanced antitumor immune responses [98]. HEK-293 cells were transfected
with retrovirus including both CTLA-4 and PD-L1- DNA plasmid, and then the cell
membranes from the transfected cells were isolated to self-assemble into an NP [98].
The NP-mediated dual inhibition of PD-L1 and CTLA-4 recruited cytotoxic CD8 +
T cells along with significant reduction of Tregs into tumors, and also increased
TNF-α secretion but decreased production of IL-6 and TGF-β [98].
5.2 CAR-T cell therapy with nanotechnology
CAR T cell therapy has revolutionized the field of immunooncology due to unprecedented therapeutic index [99]. However, the therapy is limited in scope as mentioned
previous requiring new strategies to overcome the limitations and maintain the unusual
potency of cancer immunotherapy [100]. CAR T cell therapy with nanotechnology can
broaden the applicability to various types of cancers and also maximize the therapeutic
efficacy of T cell-based anticancer therapy [100]. For instance, CAR T cell therapy with
IL-15-loaded nanogels allowed for significant elevation of tumor clearance by amplified
CAR T cells (Fig. 7) [100]. IL-15 proteins were cross-linked with redox potentialcleavable linkers to form the protein nanogel, and then the nanogels were modified with
PEG-poly(Fig. 7) [100]. The protein nanogel-embedding CAR T cells locally released the cargo
proteins across tumor tissues by increased cell surface reduction, thus remarkably increasing population of cytotoxic CD8+ T cells infiltrated into tumor and also secreting antitumor cytokines, TNF-α, IL-2, and IFN-γ into tumor compared to treatment of CAR
T cell with free IL-15 (Fig. 7) [100]. Further, the CAR T cell therapy embedded with the
IL-15 nanogel did not elevate the serum cytokine levels, IL-10, IL-6, and TNF- TNF-α
or activity of liver enzymes compared to that with free IL-15, thus minimizing the undesirable side effects with maintaining higher therapeutic efficacy [100]. As another example of CAR T cell therapy with NPs, administration of CAR T cells after NP
preconditioning was able to effectively infiltrate tumor lesions, undergo robust expansion
and kill malignant cells [101]. Although CAR T cell treatments generated cell-mediated
antitumor effect, the population of TAMs, myeloid-derived suppressor cells, Tregs were
increased, thus interrupting T cell attacks [101]. The accumulation of CAR T cells into
the tumor was highly suppressed in the solid tumor models, resulting in low antitumor
effectiveness [101]. To augment the therapeutic effectiveness of CAR T cells, RGDtagged liposome loading PI3K inhibitor and NK cell-activating agonists were systemically pretreated prior to administration of CAR T cells [101]. The liposomes were able
to reprogram tumor microenvironments by diminishing the proportion of
L-lysine and CD45 antibodies to be anchored onto the surface of CAR T cells
229Challenges and opportunities of nanotechnology in cancer immunotherapy
Fig. 7 CAR T cells combined with nanogels increased antitumor immunity to suppress tumor growth.
IL-15-loaded nanogels are anchored onto CAR T cells to induce synergistic antitumor immunity. The
nanogels release the encapsulated IL-15 via GSH- responsiveness, thus expanding cytotoxic CD8 +
T cells throughout the tumor tissues to eliminate the tumor.
immunosuppressive cells but increasing that of NK cells and CD8 + T cells [101]. After
the NP preconditioning and treatment of CAR T cells tumor progression was eradicated
and survival was doubled, attributed to the high retention of CAR T cells and infiltration
into tumors [101]. As the final example of combinational CAR T cell therapy, CAR
T cells were combined with albumin binding phospholipid-polymers enhancing
CAR T cell activity against solid tumors via the chimeric receptor [102]. Albuminbinding phospholipid-polymer tethered with CAR ligand (amph ligand) was designed
to achieve lymph node targeting by albumin-hitchhiking strategy and allow DCs to
interact with CAR T cells [102]. The successful accumulation of the amph ligands
enabled the chimeric ligands on the surface of APCs, thus priming CAR T cells
[102]. CAR T cells with vaccine boosting highly expanded T cell population and ele-
vated IFN-γ and TNF-α, thereby significantly inhibiting tumor proliferation [102].
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6. Targeting strategies
Targeting strategies affect the therapeutic efficacy of cancer immunotherapy by
boosting antitumor immunity without adverse effects. Recent advance in nanotechnology enables specific targeting delivery to the desired site augmenting the potency of antitumor immunity. In this section, we discuss several targeting approaches to drive
enhanced antitumor immunity and how nanotechnology contributes to specific
targeting.
6.1 Lymph node targeting
Lymph nodes are highly dense with APCs and consequently are a promising target to
efficiently strengthen innate immunity by delivering antigens or immunostimulatory
agents [103,104]. To facilitate lymph node targeting, the design of nanomaterials is essential, which must meet certain requirements [103,104]. First, the diameter of NPs influences how NPs drain into the lymph nodes [103,104]. NPs ranging from 10 to 100 nm
can enter through lymphatic vessels and then be retained into lymph nodes [103,104].
Second, the surface engineering of NPs strongly affects the successful accumulation of
NPs to lymph nodes, systemic circulation should be prolonged to increase the possibility
for lymph node drainage [103,104]. PEGylation of NPs is a promising strategy of surface
modification to achieve enhanced pharmacokinetics [103,104]. Lastly, the surface charge
of NPs is also important for enhanced lymph node targeting.[103, 104]The negative surface charge of NPs can block the undesirable binding to interstitum and non-target cells,
thus increasing the efficacy of lymph node targeting [103,104]. Recently, lymph node
targeting was that PEGylated NPs induced prolonged systemic circulation thereby
augmenting the possibility for lymph node drainage [105]. PEGylation of STING
agonist-loaded NPs prevented unspecific adsorption of serum proteins/matrix, which
triggered lymphatic drainage [105]. The cyclic di-GMP-loaded PEG-liposome NPs
were accumulated into lymph nodes for 2–3 days, augmenting the uptake of vaccines
and adjuvant by macrophages, DCs, and B cells [105]. The lymph node targeting delivery
highly expressed costimulatory markers in APCs, thereby inducing cytotoxic T cell
immunity to suppress tumor proliferation [105]. Furthermore, the lymph node targeting
of the NPs selectively activated lymph node-resident APCs, which did not influence on
the activation of plasmacytoid DCs, thereby minimizing the undesired cytotoxicity
[105]. The negative surface charges of NPs increased retention of the systemic circulation
and lymph node targetability. The aminiated cholesterol-grafted poly(γ-polyglutamic
acid) was mixed with ovalbumin and poly(I:C) to self-assemble into an NP [106].
The inherent negative charges of NPs triggered the retention of the NPs into lymph
nodes for up to 168 h, thereby activating DCs and NK cells in lymph nodes due to type
I IFN activation [106]. The vaccine delivery achieved by lymph node targeting significantly suppressed tumor growth and ameliorate survival [106].
Exploiting biological systems also enables effective lymph node targeting referred to as
“hitchhiking” strategy designed to interact with endogenous albumin in the bloodstream
and travel with it [107]. Albumin-binding complexes can prudentially drain lymph nodes
in that endogenous albumin drains from the interstitum and returns to the systemic circulation via lymphatic vessels [107]. Nanotechnology combined with albuminhitchhiking property can achieve lymph node targeting to reinforce both innate and
adaptive immunity [107]. In one example, albumin-binding fatty acids were conjugated
to CpG or peptide antigen, thus augmenting the accumulation of vaccine and adjuvant
into lymph nodes to boost antitumor immunity [107]. The structure of lipid-antigen or
vaccine extended the retention into lymph node for up to 150 h, which could recruit
cytotoxic CD8
+
T cells without side effects to suppress tumor proliferation [107].
Another albumin-hitchhiking strategy was that a synthetic analog, maleimidefunctionalized EB derivative, which was capable of achieving lymph node targeting
the delivery of antigen and adjuvant [44]. The maleimide-functionalized EB derivative
was able to be docked into endogenous albumin molecules, thus inducing NP formation
in serum conditions [44]. The nanovaccine surrounded by albumin molecules prolonged
its pharmacokinetic and retention time into the lymph nodes, proliferating antigenspecific CD8
+
T cells and also activating effector/central memory T cells do not only
eradicate the established tumor but also inhibit lung metastasis [44].
Utilizing magnetic responsiveness artificially rendered NPs accumulated into lymph
nodes over the long term [108]. For instance, magnetic NPs coated with CD205
antibody-tagged cancer cell membranes could be driven into lymph nodes via magnetic
fields to efficiently deliver antigen and adjuvant [108]. The magnetic NPs were retained
into lymph nodes for up to 24 days with applying magnetic fields, which could
strengthen both innate and adaptive immune responses to inhibit lung metastasis as well
as eliminate tumor progression [108].
231Challenges and opportunities of nanotechnology in cancer immunotherapy
6.2 APC targeting
APCs play an important role in mediating cellular immunity by processing and presenting
antigen recognition by certain lymphocytes such as T cells and activating adaptive immunity to drive antitumor immunity. APC targeting offers the strong possibility to initiate
antitumor immune responses and to expand antigen-specific T cells infiltrated into the
tumor via the phagocytic process. Harnessing several receptors exclusively expressed on
APCs is a promising approach to actively target APCs.
Mannose receptors overexpressed on DCs have been utilized to achieve specific targeting delivery to DCs [109]. Mannose-tagged nanomaterials are recognized as a pathogen
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by DCs, thus improving the targeting capability [109]. Mannose-tagged polymersomes
with ovalbumin and imiquimod were capable of enhancing promoting DC maturation
by delivering antigens and activating the type I IFN pathway, which was associated with
the higher uptake of vaccines by DCs [109]. The vaccine delivery via mannose receptormediated endocytosis upregulated costimulatory molecules (CD40 and CD86) and
secrete proinflammatory cytokines, thereby increasing the population of cytotoxic
T cell responses against tumor to abolish the recurrence of tumor growth [109]. Likewise,
mannose-tethered amphiphilic triblock copolymer-based NPs were selectively taken up
by DCs to deliver antigens and adjuvants [110]. The DCs specifically pulsing with the
NPs expressed the costimulatory markers, CD40, CD80, and CD86, and then activated
T cell priming to eliminate established tumor dendritic cell-specific intracellular adhesion
molecule-3-grabbing nonintegrin receptor (DC-SIGN), CD209, can be also exploited
for specific DC targeting [111]. DC-SIGN is critical in peptide presentation and eliciting
T cell activation on complementary signaling by costimulatory molecule interactions
[111] DC-SIGN antibody-tagged silica NPs were able to be engulfed by DCs compared
with the NPs without DC-SIGN [111].
The combined use of metabolic engineering and click chemistry allows for selective
DC targeting [112]. Alginate gel incorporating cytokines and azido-sugar-loaded NPs
were subcutaneously implanted to recruit DCs into the network of gels [112]. The recruited DCs exposed azido groups on their surface via the metabolism of azido sugars,
which was sensitive to click chemistry-mediated conjugation with dibenzocycloctyne
group-tethered antigen, adjuvant, or cytokine [112]. The click chemistry-mediated
DC targeting delivery significantly promoted DC maturation and secretion of
proinflammatory cytokines, thus eliciting enhanced antitumor immunity [112].
Reeducation of TAMs has been in the limelight in cancer immunotherapy as therapeutic effects are highly impeded by their antiinflammatory properties, resulting in failure of immunotherapy [113]. To modulate tumor microenvironments with
proinflammatory mode, specific TAM targeting is required by delivering immunostimulatory molecules [113]. Dextran that is one of the prevalent targeting ligands interacts with C-type lectin endowed with native macrophage avidity, which can accelerate
the preferential uptake by TAMs [113]. For example, ferumoxytol, a dextran-coated iron
oxide NP, could be preferentially taken up by TAMs and triggered M1 macrophage
polarization in vivo to suppress tumor proliferation [72]. β-cyclodextrin follows the similar behavior of dextran and also possesses the drug reservoir by host-guest interaction
[63]. β-cyclodextrin-based NPs with TLR agonists could be selectively engulfed by mac-
rophages, thereby shifting macrophages with M1 phenotype to elicit enhanced antitumor
immunity [63].
M2 targeting peptide sequences were successfully developed by library screening to
selectively target the M2 phenotype [114]. The M2 targeting peptide exclusively bound
to M2 macrophage compared to other phenotypes or other immune cells such as DCs,
B cells, and T cells [114]. When applied with the aid of nanotechnology, M2 targeting
peptide labeled on gold NPs induced the preferential uptake of the NPs by TAMs, which
modulated macrophage phenotype with M1 mode by silencing the expression of vascular
endothelial growth factor [115].
6.3 Tumor targeting
Tumor targeting delivery can improve therapeutic efficacy without adverse effects by
delivering anticancer agents at the desired site [116]. A majority of NP approaches are
mainly dependent on enhanced permeation and retention effects that have been extensively utilized in systemic delivery systems [116]. However, the enhanced permeation
and retention effect can be applied only to several tumors characterized by fast growth
rate and high angiogenic activity tumor with angiogenesis, which is not included in
the clinical model [116]. Moreover, the systemic delivery of NPs via enhanced permeation and retention effect causes a small portion of NPs to accumulate in tumor tissues,
which results in limited therapeutic potency [116]. Despite the development of various
NPs with tumor-targeting moieties, meaningful therapeutic indexes have not been
attained due to the complexity of tumor microenvironments such as high tumor intestinal fluid, slow blood flow, dense extracellular matrix, abnormal vasculature, and abundant stroma cells [116]. To reprogram tumor vasculature and extracellular matrix in and
around the tumor microenvironment for successful NP delivery, several reports
suggested that the treatment of specific antibodies could normalize environmental factors
throughout the tumor to enhance the delivery efficacy of NPs [117,118]. An additional
major challenge of NP-based cancer therapy is difficulty in penetrating and delivering
anticancer agents into a solid tumors [118]. To be efficiently accessible into a solid tumor,
again the normalization of tumor microenvironments are required by treating the antibodies that suppressing angiogenesis and extracellular matrix formation [118]. The treatment of VEGF antibody significantly reduces vessel density, vessel tortuosity, and leakage
fraction along with increasing pericyte coverage [118]. In addition, the administration of
TGF-β antibody decreased the extracellular matrix contents, thus increasing the accessibility of NPs into the tumor [118]. The combination of these two treatments highly
improved the NP delivery into tumors even within depths of the tumor tissue by remodeling of tumor microenvironments [118].
Intratumoral delivery is the most straightforward method to deliver therapeutic agents
directly into tumor only if the tumor is accessible, which showed higher therapeutic
effects compared to systemic delivery [1]. The intratumoral injection can bypass several
critical hurdles until tumor entry, thus achieving a dose-sparing effect and minimizing
off-target delivery [1]. Although intratumoral delivery directly accumulates NPs into
tumor, the retention of NPs into the tumors is not certain. To augment the retention
time of NPs into the tumor, NPs tethered with extracellular matrix-binding peptides
adhere to extracellular matrix collagen, thus increasing the therapeutic efficacy without
causing adverse events [119].
233Challenges and opportunities of nanotechnology in cancer immunotherapy
234 DaeYong Lee et al.
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7. Perspective
Immunotherapy with nanotechnology possesses huge potential to overcome the
current critical limitations in cancer immunotherapy. The treatment of immune checkpoint inhibitors alone does not efficiently sensitize antitumor immunity, thus providing
the impetus to harness nanotechnology for effective cancer therapy. NPs allow tumor
microenvironments to be modulated to more tumor-suppressive modes by awakening
innate or adaptive immunity. The combinational therapy of immune checkpoint
blockers with NPs synergistically amplified robust and long-term antitumor immunity,
thereby suppressing tumor proliferation and also metastasis to other organs. Moreover,
CAR-T cell therapies that have been recently revolutionized are highly restricted in most
solid tumors despite unprecedented therapeutic indexes achieved in the clinical study.
However, CAR T cell therapy with nanotechnology is capable of addressing the crucial
hurdle by reprogramming tumor microenvironments and sensitizing immune cells
against tumor cells. Immunotherapy with the aid of nanotechnology may provide a significant breakthrough in cancer treatment. However, numerous NP-based strategies
have failed to be translated into clinical models. The perpetual development of NPs
aimed for enhanced cancer immunotherapy is required to establish a new platform in
immunooncology.
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