Myeloid-T cell interplay and cell state transitions associated with checkpoint inhibitor response in melanoma.

T cell Translation to patients cancer immunotherapy immune checkpoint macrophage melanoma peripheral blood mononuclear cell single-cell RNA sequencing tumor microenvironment tumor-infiltrated lymphocyte

Journal

Med (New York, N.Y.)
ISSN: 2666-6340
Titre abrégé: Med
Pays: United States
ID NLM: 101769215

Informations de publication

Date de publication:
04 Apr 2024
Historique:
received: 14 06 2023
revised: 23 11 2023
accepted: 17 03 2024
medline: 10 4 2024
pubmed: 10 4 2024
entrez: 9 4 2024
Statut: aheadofprint

Résumé

The treatment of melanoma, the deadliest form of skin cancer, has greatly benefited from immunotherapy. However, many patients do not show a durable response, which is only partially explained by known resistance mechanisms. We performed single-cell RNA sequencing of tumor immune infiltrates and matched peripheral blood mononuclear cells of 22 checkpoint inhibitor (CPI)-naive stage III-IV metastatic melanoma patients. After sample collection, the same patients received CPI treatment, and their response was assessed. CPI responders showed high levels of classical monocytes in peripheral blood, which preferentially transitioned toward CXCL9-expressing macrophages in tumors. Trajectories of tumor-infiltrating CD8 Our study illustrates that the tumor immune microenvironment prior to CPI treatment can be indicative of response. In perspective, modulating the myeloid and/or effector cell compartment by altering the described cell interactions and transitions could improve immunotherapy response. This research was funded by Roche Pharma Research and Early Development.

Sections du résumé

BACKGROUND BACKGROUND
The treatment of melanoma, the deadliest form of skin cancer, has greatly benefited from immunotherapy. However, many patients do not show a durable response, which is only partially explained by known resistance mechanisms.
METHODS METHODS
We performed single-cell RNA sequencing of tumor immune infiltrates and matched peripheral blood mononuclear cells of 22 checkpoint inhibitor (CPI)-naive stage III-IV metastatic melanoma patients. After sample collection, the same patients received CPI treatment, and their response was assessed.
FINDINGS RESULTS
CPI responders showed high levels of classical monocytes in peripheral blood, which preferentially transitioned toward CXCL9-expressing macrophages in tumors. Trajectories of tumor-infiltrating CD8
CONCLUSIONS CONCLUSIONS
Our study illustrates that the tumor immune microenvironment prior to CPI treatment can be indicative of response. In perspective, modulating the myeloid and/or effector cell compartment by altering the described cell interactions and transitions could improve immunotherapy response.
FUNDING BACKGROUND
This research was funded by Roche Pharma Research and Early Development.

Identifiants

pubmed: 38593812
pii: S2666-6340(24)00127-2
doi: 10.1016/j.medj.2024.03.015
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests R.S., S. Hoves, M.B., T.H., S.D., E.Y., F.L., S. Herter, P.U., A.I., J.S., J.S.-P., T.K.-T., I.G.d.M., and P.C.S. are employed by and hold F. Hoffmann-La Roche Ltd. company stock. P.U. and M.B. disclose ownership of F. Hoffmann-La Roche Ltd. patents. R.D. has intermittent, project-focused consulting and/or advisory relationships with Novartis, Merck Sharp & Dohme (MSD), Bristol-Myers Squibb (BMS), Roche, Amgen, Takeda, Pierre Fabre, Sun Pharma, Sanofi, Catalym, Second Genome, Regeneron, Alligator, T3 Pharma, MaxiVAX SA, Pfizer, and touchIME outside of the submitted work. M.P.L. receives project-specific research support outside of the scope of this work from Roche, Novartis, Molecular Partners, and Oncobit.

Auteurs

Ramona Schlenker (R)

Roche Innovation Center Munich, Roche Pharma Research and Early Development (pRED), Penzberg, Germany. Electronic address: ramona.schlenker@roche.com.

Petra C Schwalie (PC)

Roche Innovation Center Basel, pRED, Basel, Switzerland. Electronic address: petra.schwalie@roche.com.

Steffen Dettling (S)

Roche Innovation Center Munich, Roche Pharma Research and Early Development (pRED), Penzberg, Germany.

Tamara Huesser (T)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Anja Irmisch (A)

Department of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Marisa Mariani (M)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Julia M Martínez Gómez (JM)

Department of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Alison Ribeiro (A)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Florian Limani (F)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Sylvia Herter (S)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Emilio Yángüez (E)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Sabine Hoves (S)

Roche Innovation Center Munich, Roche Pharma Research and Early Development (pRED), Penzberg, Germany.

Jitka Somandin (J)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Juliane Siebourg-Polster (J)

Roche Innovation Center Basel, pRED, Basel, Switzerland.

Tony Kam-Thong (T)

Roche Innovation Center Basel, pRED, Basel, Switzerland.

Ines Grazina de Matos (IG)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Pablo Umana (P)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Reinhard Dummer (R)

Department of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Mitchell P Levesque (MP)

Department of Dermatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Marina Bacac (M)

Roche Innovation Center Zurich, pRED, Schlieren, Switzerland.

Classifications MeSH