Subverting the adaptive immune resistance mechanism to improve clinical responses to immune checkpoint blockade therapy

Young J. Kim

doi:10.4161/21624011.2014.954868

Subverting the adaptive immune resistance mechanism to improve clinical responses to immune checkpoint blockade therapy

Young J. Kim

School of Medicine

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

Abstract

The correlation between tumor-infiltrating lymphocyte (TIL)-expression of programmed cell death ligand 1 (PD-L1) and clinical responsiveness to the PD-1 blocking antibody nivolumab implicates adaptive immune evasion mechanisms in cancer. We review our findings that tumor cell PD-L1 expression is induced by interferon γ (IFNγ) producing TILs. We provide a mechanistic rationale for combining IFNγ⁺ T helper type 1 (Th1)-inducing cancer vaccines with PD-1 immune checkpoint blockade.

Original language	English (US)
Pages (from-to)	1-2
Number of pages	2
Journal	OncoImmunology
Volume	3
Issue number	12
DOIs	https://doi.org/10.4161/21624011.2014.954868
State	Published - Dec 2 2014

Keywords

adaptive immune resistance
anti-PD-1
cancer vaccine
TLR agonists
tumor microenvironment

ASJC Scopus subject areas

Immunology and Allergy
Oncology
Immunology

Access to Document

10.4161/21624011.2014.954868

Cite this

@article{b60887dedc554499b8e02e459fb0f1e5,

title = "Subverting the adaptive immune resistance mechanism to improve clinical responses to immune checkpoint blockade therapy",

abstract = "The correlation between tumor-infiltrating lymphocyte (TIL)-expression of programmed cell death ligand 1 (PD-L1) and clinical responsiveness to the PD-1 blocking antibody nivolumab implicates adaptive immune evasion mechanisms in cancer. We review our findings that tumor cell PD-L1 expression is induced by interferon γ (IFNγ) producing TILs. We provide a mechanistic rationale for combining IFNγ+ T helper type 1 (Th1)-inducing cancer vaccines with PD-1 immune checkpoint blockade.",

keywords = "adaptive immune resistance, anti-PD-1, cancer vaccine, TLR agonists, tumor microenvironment",

author = "Kim, {Young J.}",

year = "2014",

month = dec,

day = "2",

doi = "10.4161/21624011.2014.954868",

language = "English (US)",

volume = "3",

pages = "1--2",

journal = "OncoImmunology",

issn = "2162-4011",

publisher = "Landes Bioscience",

number = "12",

}

TY - JOUR

T1 - Subverting the adaptive immune resistance mechanism to improve clinical responses to immune checkpoint blockade therapy

AU - Kim, Young J.

PY - 2014/12/2

Y1 - 2014/12/2

N2 - The correlation between tumor-infiltrating lymphocyte (TIL)-expression of programmed cell death ligand 1 (PD-L1) and clinical responsiveness to the PD-1 blocking antibody nivolumab implicates adaptive immune evasion mechanisms in cancer. We review our findings that tumor cell PD-L1 expression is induced by interferon γ (IFNγ) producing TILs. We provide a mechanistic rationale for combining IFNγ+ T helper type 1 (Th1)-inducing cancer vaccines with PD-1 immune checkpoint blockade.

AB - The correlation between tumor-infiltrating lymphocyte (TIL)-expression of programmed cell death ligand 1 (PD-L1) and clinical responsiveness to the PD-1 blocking antibody nivolumab implicates adaptive immune evasion mechanisms in cancer. We review our findings that tumor cell PD-L1 expression is induced by interferon γ (IFNγ) producing TILs. We provide a mechanistic rationale for combining IFNγ+ T helper type 1 (Th1)-inducing cancer vaccines with PD-1 immune checkpoint blockade.

KW - adaptive immune resistance

KW - anti-PD-1

KW - cancer vaccine

KW - TLR agonists

KW - tumor microenvironment

UR - http://www.scopus.com/inward/record.url?scp=84938777895&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84938777895&partnerID=8YFLogxK

U2 - 10.4161/21624011.2014.954868

DO - 10.4161/21624011.2014.954868

M3 - Article

C2 - 25964860

AN - SCOPUS:84938777895

SN - 2162-4011

VL - 3

SP - 1

EP - 2

JO - OncoImmunology

JF - OncoImmunology

IS - 12

ER -

Subverting the adaptive immune resistance mechanism to improve clinical responses to immune checkpoint blockade therapy

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this