Good cops turn bad: The contribution of neutrophils to immune-checkpoint inhibitor treatment failures in cancer

Immune checkpoint inhibitor therapy activates tumor-killing T-cells by releasing the brake of anti-tumor immunity. It has been approved as first- or second-line therapy in many cancer types. Unfortunately, a majority of immune checkpoint inhibitor recipients are refractory to the therapy. Recent inv...

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Bibliographic Details
Published inPharmacology & therapeutics (Oxford) Vol. 217; p. 107662
Main Authors Zhang, Huajia, Houghton, A. McGarry
Format Journal Article
LanguageEnglish
Published England Elsevier Inc 01.01.2021
Subjects
Immune checkpoint inhibitor
Neutrophil
PMN-MDSC
TME
CXCL
NO
MDSC
Immune checkpoint inhibitor
MPO
PI3K
PMN-MDSC
PD-L1
iNOS
CTLA-4
NSCLC
TME
ICI
ECM
PMN
L-Arg
MMP
PB
NE
ROS
Arg
Neutrophil
CXCR
NET
PD-1
MRC
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Summary:Immune checkpoint inhibitor therapy activates tumor-killing T-cells by releasing the brake of anti-tumor immunity. It has been approved as first- or second-line therapy in many cancer types. Unfortunately, a majority of immune checkpoint inhibitor recipients are refractory to the therapy. Recent investigations of the peripheral blood and tumor microenvironment of cancer patients indicate that high neutrophil content is associated with poor response rates, suggesting an opportunity for synergistic therapy. In the current review, we discuss the mechanisms of neutrophil-mediated immunosuppression in cancer and recent findings suggesting that neutrophil antagonism will improve the efficacy of immune checkpoint inhibitor therapy.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:0163-7258
1879-016X
DOI:10.1016/j.pharmthera.2020.107662