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278 Kai Shi
melanoma as well as a considerable proportion of bone and soft tissue sarcomas [187].In
contrast, the expression of FAP is limited to the fibroblasts of the wound and developing
fetus in normal human tissues. This highly selective expression of FAP in CAFs indicates
that it is likely to be an ideal stroma antigen candidate for cancer immunotherapy [188].
As early as 2005, Lee et al. transfected the mRNA encoding FAP into murine bone
marrow-derived DCs by electroporation in vitro, and induced maturation of DCs with lipopolysaccharide (100 ng/mL) as an adjuvant. Upon receiving two immunizations by intraperitoneal inoculation of DCs vaccines, the tumor growth of mice bearing B16/F10.9
melanoma was significantly retarded [189]. Interestingly, the responseintensity of FAP vaccination was comparableto that of the tumor antigenTrp-2. Considering that melanoma is a
tumor model with low expression of MHC class I, they further modified the vaccine by
attaching the lysosome targeted signal sequence of LAMP-1 to the FAP encoded mRNA,
which could redirect the transcribed FAP antigeninto the classII presentation pathway, and
furtherstimulate CD4
+
T cells mediated antitumorimmuneresponse.It shouldbe notedthat
the antigenic targets in tumor stroma generally appear as autoantigens, which are normal
nonmutated gene expressions, and they are preferentially but not necessarily exclusively
expressed in stromal cells. This raises concerns that vaccination against stromalantigens such
as FAP will induce autoimmune pathology. In this study, no morbidity or mortality associated with anti-FAP vaccination was observed, except that wound healing was slightly delayed, which is consistent with the expression of FAP in wounds. This study shows that
vaccination against this normal product can induce protective antitumor immunity in the
absence of obvious autoimmunity, except for the small delay of wound healing, which is
related to the induction of FAP-specific immune response. Overall, these observations suggest that vaccination against stromal products such as FAP can elicit protective antitumor
immunity in the absence of unacceptable levels of autoimmune pathology. Recently, Xie
et al. constructed a recombinant adenovirus vector that packaged cDNA-encoding mouse
FAP-αof CAFs(rAd-FAP-α)[190]. C57BL/6micereceivedimmunization by s.c.injection
of bone marrow-derived DCs that have been infected with rAd-FAP-α.Theresultsshowed
that the immunization with adenovirus vector vaccine against FAP-α triggered powerful
FAP-αspecificcytotoxic T lymphocytes, whichwere capableof lysingCAFs in mice bearing
Lewis lung cancer. In addition, compared with the control group, the vaccinated mice
obtained effective therapeutic or protective antitumor immunity, as well as prolonged overall survival time.
Due to the heterogeneous expression of antigens in tumors, most immunotherapies
using monovalent vaccines often suffer from limited therapeutic efficacy. Therefore, the
employment of multivalent vaccines to target multiple distinct tumor-associated antigens
may induce a synergistic activation response of polyclonal T cells, thereby avoiding
tumor immune escape caused by antigen loss. Fang et al. first studied the tumor preventive effect of lentiviral vaccines (termed LV-3Ag) that encoded three tumor-associated
antigens, including glycoprotein 100 (gp100), tyrosinase-related protein 1 (TRP1),
and tyrosinase-related protein 2 (TRP2), by a prophylactic protocol against melanoma
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[191]. In the study, C57BL/6 mice were vaccinated with LV-3Ag by s.c administration
and challenged by s.c. inoculation of B16F10 melanoma cells 10 days after boost immunization. The results showed that LV-3Ag immunization provided mice a stronger
tumor-protective immune function. Compared with the control group, all animals in
the immunized group showed significant suppression of tumor progression. However,
the experimental results also showed that compared to its capacity of preventing tumor
progression in the prophylactic melanoma model, immunization with LV-3Ag alone was
less effective for retarding the growth of established melanoma in a therapeutic model. To
this end, a novel immunotoxin termed αFAP-PE38 that targeting FAP-positive fibroblasts within the tumor stroma was engineered for synergistic immunotherapy with
LV-3Ag. Indeed, the elimination of CAFs with αFAP-PE38 allowed enhanced tumor
inhibition of LV-3Ag in the established B16 melanoma model. In particular, a significant
increase in the ratio of CD8 + T cells relative to Tregs and MDSCs in the group receiving the combination treatment was observed. These findings suggested that targeting
within the tumor stroma could attenuate the immunosuppressive tumor microenvironment, leading to more CTLs activation and promoting the production of Th1-type cytokines such as IL-2, IL-12, and TNF-α, thereby yielding improved therapeutic outcome
(Table 1).
279Stromal modulation strategies
Table 1 Summarized stromal modulation strategies based on nanoparticles to improve
immunotherapy response in cancer.
Stromal
Strategies
Vasculature
normalization
ECM remodeling TGF-β,
targets
VEGFR-2 Quantum dot α-VEGFR-2 [146, 147]
Integrin
αvβ3
ANG-2,
VEGF-A
VE-cadherin Au/PEG-PDEAEA Au [151]
VEGFR2,
MCT4
HEVs,
TN-C
collagen
TGF-β,
collagen
Collagen Liposome Collagenase [161]
TGF-β,
collagen
Nanoparticulate
compositions
PHis-PGA RGD peptide [148]
Bispecific antibody α-ANG-2, α-VEGF-A [149]
Chitosan Apatinib, lonidamine [152]
Calcium phosphate
liposomes
Liposome Losartan [157]
Polyacetals Valsartan [159]
Lipid-calcium-
phosphate
Immunomodulatory
payloads Reference
LIGHT, α-mangiferin [153]
Relaxin [162, 163]
Continued
280 Kai Shi
Table 1 Summarized stromal modulation strategies based on nanoparticles to improve
immunotherapy response in cancer—cont’d
Strategies
Stromal
targets
Nanoparticulate
compositions
Immunomodulatory
payloads Reference
Hyaluronic
acid
Hyaluronic
acid
Hyaluronic
acid
CAFs depletion SMA Carboxymethyl
TGF-β Gelatin, Pt Telmisartan, paclitaxel [171]
Wnt16 PLL-PEG-PCL 18β-glycyrrhetinic acid,
FAP Oncolytic
FAP mAb-IR700 α-FAP, IR700 [176]
FAP Apolipoferritin α-FAP, ZnF16Pc [177]
Blocking CAFs
crosstalk
Reprogramming
CAFs
Against stromal
antigens
CXCL12 Protamine-liposome pCXCL12 trap [178]
CXCL12 Lipid calcium
Wnt16 Lipid calcium
ROS Nanoemulsion Puerarin [184]
TGF-β Nanoemulsion Fraxinellone [185]
FAP DCs vaccine cDNA encoding FAP-α [190]
FAP Lentiviral vaccine Gp100, TRP1/2 [191]
PLGA-PEG Hyaluronidase [166]
PEI/CpG/OVA Hyaluronidase [167]
Dextran Hyaluronidase [169]
cellulose
adenovirus
phosphate
phosphate
Docetaxel [170]
[172]
gemcitabine
α-FAP [173]
pCXCL12 trap [179]
Quercetin [183]
4. Conclusions
In cooperation with immunology and materials science, a series of novel immunomodulatory nanoparticles are being developed for tumor immunotherapy. They provide an attractive delivery method for targeted modulation of tumor stroma and are
responsible for effectively protecting vaccines and immunomodulatory molecules from
degradation, improving biodistribution and pharmacokinetics in vivo, as well as increasing
their accumulation within tumor sites. In addition, they are capable of specifically
targeting various tumor stromal components, and perform local immune regulation
therein, accordingly enhancing the efficacy of tumor immunotherapy while reducing
systemic immunotoxicity.
The tumor stroma is an extremely complex network in which there are crosstalks
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among immune cells, stromal cells, and tumor cells via various autocrine and paracrine
signaling pathways as well as direct action. We currently lack a comprehensive understanding of the immune regulation mechanisms of tumors, which is why we are encountering a considerable of difficulties and confusion when attempting to solve antitumor
issues from an immune perspective. An in-depth understanding of the crosstalks and
immunological attributes of the infiltrating components within the tumor stroma will
help to provide more immunotherapeutic targets for stromal modulation of nanoparticles
and lay the foundation for the construction of intelligent nanomedicine delivery systems
with environmental responsiveness. Further elucidating the dynamic network of stromal
signals facilitating immune tolerance and tumor evasion from immune surveillance is
expected to help guide the implementation of new stromal immunomodulation strategies
by nanoparticles, and more effectively relieve the suppressive effect of tumor stroma
milieu on immunotherapy.
In the prospective research work on tumor immunotherapy, nanoparticles with multiple stromal stimuli responsiveness (for instance, extracellular acidity, hypoxia, and
matrix enzymes) and external stimulus responsiveness such as photothermal and photoacoustic will emerge as hot research directions, which are expected to overcome a variety
of physiological barriers encountered while delivering immunomodulators in vivo. Nevertheless, these environmental stimuli-responsive nanoparticles also have issues related to
their complicated design and the synthesis of carrier materials, such as difficulty in quality
control. It is believed that with the continuous development of materials science, oncology and immunology, these issues will be solved effectively, and intelligent nanoparticles
will be developed toward the direction of more rational design and precise targeting. The
combination of cancer immunology and nanotechnology is becoming an emerging field
in biomedical science.
281Stromal modulation strategies
Acknowledgments
The authors thank the National Natural Science Foundation of China (No. 81971729) for financial support.
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