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2016 ; 5
(11
): e1230578
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TLR7-based cancer immunotherapy decreases intratumoral myeloid-derived suppressor
cells and blocks their immunosuppressive function
#MMPMID27999739
Spinetti T
; Spagnuolo L
; Mottas I
; Secondini C
; Treinies M
; Rüegg C
; Hotz C
; Bourquin C
Oncoimmunology
2016[]; 5
(11
): e1230578
PMID27999739
show ga
Myeloid-derived suppressor cells (MDSC) are a heterogeneous population of
immature myeloid cells with the capacity to inhibit immunological responses.
During cancer progression, MDSC are recruited to the tumor sites and secondary
lymphoid organs, leading to the suppression of the antitumor function of NK and T
cells. Here, we show that the TLR7/8 agonist resiquimod (R848) has a direct
effect on MDSC populations in tumor-bearing mice. Systemic application of R848
led to a rapid reduction in both intratumoral and circulating MDSC. The
subpopulation of monocytic MDSC (m-MDSC) was the most affected by R848 treatment
with an up to 5-fold decrease in the tumor. We found that TLR7 stimulation in
tumor-bearing mice led to a maturation and differentiation of MDSC with
upregulation of the surface molecules CD11c, F4/80, MHC-I, and MHC-II. MDSC
treated with R848 lost their immunosuppressive function and acquired instead an
antigen-presenting phenotype with the capability to induce specific T-cell
proliferation. Importantly, we found that MDSC co-injected s.c. with CT26 tumor
cells lost their ability to support tumor growth after pretreatment with R848.
Our results demonstrate that treatment of tumor-bearing mice with a TLR7/8
agonist acts directly on MDSC to induce their maturation and leads them to
acquire a non-suppressive status. Considering the obstacles posed by MDSC for
cancer immunotherapy, targeting these cells by a TLR7/8 agonist may improve
immune responses against cancer.
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