Common phenotypic dynamics of tumor-infiltrating lymphocytes across different histologies upon checkpoint inhibition: impact on clinical outcome.


Journal

Cytotherapy
ISSN: 1477-2566
Titre abrégé: Cytotherapy
Pays: England
ID NLM: 100895309

Informations de publication

Date de publication:
04 2020
Historique:
received: 25 09 2019
revised: 18 12 2019
accepted: 22 01 2020
pubmed: 24 3 2020
medline: 28 10 2020
entrez: 24 3 2020
Statut: ppublish

Résumé

Immune checkpoint inhibitors (ICIs) have revolutionized the cancer therapeutic landscape and our perception of interactions between the immune system and tumor cells. Despite remarkable progress, disease relapse and primary resistance are not uncommon. Understanding the biological processes that tumor-infiltrating lymphocytes (TILs) undergo during ICI, how this affects the tumor microenvironment (TME) and, ultimately, clinical outcome is, therefore, necessary to further improve treatment efficacy. In the current study, we sought to characterize TILs from patients with metastatic solid tumors undergoing ICI correlating flowcytometric findings with clinical outcome. In total, 20 patients with 10 different metastatic solid tumors treated with ICIs targeting programmed-cell death-1 (PD-1)/PD-L1 axis were included in this study. The phenotype of T cells deriving from biopsies obtained prior to treatment initiation and on-treatment was investigaded. Analyses were focused on T cells' degree of differentiation and activity and how they correlate with transcriptomic changes in the TME. Data indicate that patients benefitting from ICIs accumulate CD8+central memory T cells. TILs developed an effector-like phenotype over time, which was also associated with a cytolytic gene signature. In terms of modulation of T-cell responses, we observed that high expression of checkpoint molecules pre-treatment (i.e., PD-1, lymphocyte activation gene-3 [LAG-3], B and T-lymphocyte attenuator [BTLA] and T-cell immunoglobulin and mucin domain containing-3 [TIM-3]) was associated with similar gene signature and correlated to treatment benefit. Increasing expression of LAG-3 and BTLA in the CD8 compartment and their co-expression with PD-1 during treatment were, however, a common feature for patients who failed to respond to ICIs. Besides identifying immune profiles suggestive of response to ICI, our results provide a more nuanced picture regarding expression of checkpoint molecules that goes beyond T-cell anergy.

Sections du résumé

BACKGROUND
Immune checkpoint inhibitors (ICIs) have revolutionized the cancer therapeutic landscape and our perception of interactions between the immune system and tumor cells. Despite remarkable progress, disease relapse and primary resistance are not uncommon. Understanding the biological processes that tumor-infiltrating lymphocytes (TILs) undergo during ICI, how this affects the tumor microenvironment (TME) and, ultimately, clinical outcome is, therefore, necessary to further improve treatment efficacy.
AIM
In the current study, we sought to characterize TILs from patients with metastatic solid tumors undergoing ICI correlating flowcytometric findings with clinical outcome.
METHODS
In total, 20 patients with 10 different metastatic solid tumors treated with ICIs targeting programmed-cell death-1 (PD-1)/PD-L1 axis were included in this study. The phenotype of T cells deriving from biopsies obtained prior to treatment initiation and on-treatment was investigaded. Analyses were focused on T cells' degree of differentiation and activity and how they correlate with transcriptomic changes in the TME.
RESULTS
Data indicate that patients benefitting from ICIs accumulate CD8+central memory T cells. TILs developed an effector-like phenotype over time, which was also associated with a cytolytic gene signature. In terms of modulation of T-cell responses, we observed that high expression of checkpoint molecules pre-treatment (i.e., PD-1, lymphocyte activation gene-3 [LAG-3], B and T-lymphocyte attenuator [BTLA] and T-cell immunoglobulin and mucin domain containing-3 [TIM-3]) was associated with similar gene signature and correlated to treatment benefit. Increasing expression of LAG-3 and BTLA in the CD8 compartment and their co-expression with PD-1 during treatment were, however, a common feature for patients who failed to respond to ICIs.
CONCLUSIONS
Besides identifying immune profiles suggestive of response to ICI, our results provide a more nuanced picture regarding expression of checkpoint molecules that goes beyond T-cell anergy.

Identifiants

pubmed: 32201034
pii: S1465-3249(20)30014-1
doi: 10.1016/j.jcyt.2020.01.010
pii:
doi:

Substances chimiques

B7-H1 Antigen 0
CD274 protein, human 0
Immunologic Factors 0
PDCD1 protein, human 0
Programmed Cell Death 1 Receptor 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

204-213

Informations de copyright

Copyright © 2020 International Society for Cell and Gene Therapy. Published by Elsevier Inc. All rights reserved.

Auteurs

Vinicius Araujo B de Lima (V)

Rigshospitalet, Department of Oncology, Phase 1 Unit, Copenhagen, Denmark. Electronic address: vinicius.araujo.barbosa.de.lima@regionh.dk.

Annie Borch (A)

Department of Health Technology, Technical University of Denmark, Lyngby, Denmark.

Morten Hansen (M)

National Center for Cancer Immune Therapy, Department of Oncology, Herlev Hospital, Herlev, Denmark.

Arianna Draghi (A)

National Center for Cancer Immune Therapy, Department of Oncology, Herlev Hospital, Herlev, Denmark.

Iben Spanggaard (I)

Rigshospitalet, Department of Oncology, Phase 1 Unit, Copenhagen, Denmark.

Kristoffer Rohrberg (K)

Rigshospitalet, Department of Oncology, Phase 1 Unit, Copenhagen, Denmark.

Sine Reker Hadrup (S)

Department of Health Technology, Technical University of Denmark, Lyngby, Denmark.

Ulrik Lassen (U)

Rigshospitalet, Department of Oncology, Phase 1 Unit, Copenhagen, Denmark.

Inge Marie Svane (IM)

National Center for Cancer Immune Therapy, Department of Oncology, Herlev Hospital, Herlev, Denmark.

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Classifications MeSH