Evidence map›Paper›PMID 32179637›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2020

Cancer Cell-Intrinsic Expression of MHC Class II Regulates the Immune Microenvironment and Response to Anti-PD-1 Therapy in Lung Adenocarcinoma.

Amber M Johnson, Bonnie L Bullock, Alexander J Neuwelt, Joanna M Poczobutt, Rachael E Kaspar, Howard Y Li, Jeff W Kwak, Katharina Hopp, Mary C M Weiser-Evans, Lynn E Heasley and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 131 citations in OpenAlex.

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  9. Enhanced antitumor efficacy of combined targeting of adenosine ACancer immunology, immunotherapy : CII · 2026
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35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Amber M JohnsonDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.ORCID 0000-0002-5392-8705
Bonnie L BullockDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Alexander J NeuweltDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Joanna M PoczobuttDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Rachael E KasparDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.ORCID 0000-0002-1181-7919
Howard Y LiDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Jeff W KwakDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.ORCID 0000-0003-1481-3654
Katharina HoppDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Mary C M Weiser-EvansDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Lynn E HeasleyDepartment of Veterans Affairs Medical Center, Denver, CO 80220.
Erin L SchenkDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.ORCID 0000-0001-9418-9948
Eric T ClambeyDepartment of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.ORCID 0000-0002-7972-9544
Raphael A NemenoffDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045; raphael.nemenoff@cuanschutz.edu.ORCID 0000-0002-2369-2535
University of Colorado Anschutz Medical Campus · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Paul Calabresis Award in Clinical Oncology ResearchK12CA086913 · NCI · UNIVERSITY OF COLORADO DENVER · PI VIRGINIA F. BORGES, Jill E Slansky · 2000 to 2026
$17.8M
VASOPRESSIN SIGNAL TRANSDUCTION IN SMALL CELL LUNG CANCERP01DK019928 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BERL, TOMAS · 1986 to 2008
$11.8M
Training in Translational Research of Lung, Head and Neck CancerT32CA174648 · NCI · UNIVERSITY OF COLORADO DENVER · PI KARAM, SANA D · 2013 to 2022
$4.2M
Effects of Complement on the Tumor Microenvironment in Lung CancerR01CA236222 · NCI · UNIVERSITY OF COLORADO DENVER · PI NEMENOFF, RAPHAEL A., THURMAN, JOSHUA M · 2019 to 2023
$2.0M
Eicosanoids in Lung Cancer: Progression and MetastasisR01CA162226 · NCI · UNIVERSITY OF COLORADO DENVER · PI NEMENOFF, RAPHAEL A. · 2013 to 2017
$1.6M
NCATS NIH HHS UL1 TR001082NCI NIH HHS K12 CA086913NCI NIH HHS P30 CA046934NCI NIH HHS P50 CA058187NCI NIH HHS R01 CA162226NCI NIH HHS R01 CA236222NCI NIH HHS T32 CA174648NIDDK NIH HHS P01 DK019928
6 · The paper itself

Abstract

MHC class II (MHCII) expression is usually restricted to APC but can be expressed by cancer cells. We examined the effect of cancer cell-specific MHCII (csMHCII) expression in lung adenocarcinoma on T cell recruitment to tumors and response to anti-PD-1 therapy using two orthotopic immunocompetent murine models of non-small cell lung cancer: CMT167 (CMT) and Lewis lung carcinoma (LLC). We previously showed that CMT167 tumors are eradicated by anti-PD1 therapy, whereas LLC tumors are resistant. RNA sequencing analysis of cancer cells recovered from tumors revealed that csMHCII correlated with response to anti-PD1 therapy, with immunotherapy-sensitive CMT167 cells being csMHCII positive, whereas resistant LLC cells were csMHCII negative. To test the functional effects of csMHCII, MHCII expression was altered on the cancer cells through loss- and gain-of-function of CIITA, a master regulator of the MHCII pathway. Loss of CIITA in CMT167 decreased csMHCII and converted tumors from anti-PD-1 sensitive to anti-PD-1 resistant. This was associated with lower levels of Th1 cytokines, decreased T cell infiltration, increased B cell numbers, and decreased macrophage recruitment. Conversely, overexpression of CIITA in LLC cells resulted in csMHCII in vitro and in vivo. Enforced expression of CIITA increased T cell infiltration and sensitized tumors to anti-PD-1 therapy. csMHCII expression was also examined in a subset of surgically resected human lung adenocarcinomas by multispectral imaging, which provided a survival benefit and positively correlated with T cell infiltration. These studies demonstrate a functional role for csMHCII in regulating T cell infiltration and sensitivity to anti-PD-1.

Indexed as

Adenocarcinoma of LungAnimalsDisease Models, AnimalHistocompatibility Antigens Class IILung NeoplasmsMaleMiceMice, Inbred C57BLNuclear ProteinsProgrammed Cell Death 1 ReceptorTrans-ActivatorsTumor MicroenvironmentHistocompatibility Antigens Class IIMHC class II transactivator proteinNuclear ProteinsPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorTrans-Activators

Identifiers

PMID32179637
PMCPMC7472648
OpenAlexW3012475590

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.