Mast-cell derived nerve growth factor drives ILC2 pro-tumoral functions in bladder cancer

M Maryline Falquet H Hajar El Ahanidi A Alejandra Gomez-Cadena Z Ziyang Su A Anthony Cornu T Tania Wyss B Burak Kizil R Robert Pick (Department of Pathology and Immunology, Faculty of Medicine, University of Geneva) K Katayoun Falamaki P Pratyaksha Wirapati B Benedetta Fiordi I Isis Senoner D Daniela Claudia Maresca N Neil Kallal D Danaé Guedj M Mario Kreutzfeldt J Jean-Christophe Tille M Marine M. Leblond K Katarzyna Michaud S Silvia Pesce S Simona Candiani K Korneliusz Golebski J Julien Dagher M Melinda Charrier C Caroline Pressacco Brossier E Elisabeth Grobet-Jeandin R Romina Marone S Stéphanie Hugues L Lukas T. Jeker G Grégory Verdeil D Doron Merkler (Department of Pathology and Immunology, Faculty of Medicine, University of Geneva) E Emanuela Marcenaro C Christoph Scheiermann M Mohammed Attaleb D Daniel Benamran P Petros Tsantoulis G Giuseppe Ercolano S Sara Trabanelli C Camilla Jandus

Abstract

Abstract Innate lymphoid cells type 2 (ILC2s) are key regulators of tissue homeostasis and inflammation. In cancer, ILC2s can exhibit pro-tumoral functions by increasing the myeloid derived suppressor cells (MDSC)/T-cell ratio. Nevertheless, the upstream ILC2 triggers remain poorly defined. Here, we identify nerve growth factor (NGF) as the driver of ILC2 pro-tumoral functions in patients with bladder cancer. We show that ILC2s express the NGF receptor TrkA and respond to NGF by secreting type-2 cytokines. In the tumor microenvironment, NGF-producing mast cells accumulate and activate ILC2s to induce regulatory T cells (Tregs), ultimately fostering tumor growth. In patients, NGF levels inversely correlate with survival in ILC2-rich tumors, underscoring the clinical significance of this axis. In vivo administration of a selective TrkA inhibitor improves survival in orthotopic tumor-bearing female mice and sensitizes them to immune checkpoint blockade (ICB). Overall, we identify NGF as an ILC2 activator that shapes pro-tumoral ILC2 functions. The blockade of TrkA + ILC2s might represent a targetable strategy to improve survival, particularly in ICB-resistant patients.

Article Details

Volume / Issue Vol. 17, Issue 1
Published February 21, 2026
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (39)

M

Maryline Falquet

H

Hajar El Ahanidi

A

Alejandra Gomez-Cadena

Z

Ziyang Su

A

Anthony Cornu

T

Tania Wyss

B

Burak Kizil

R

Robert Pick

Department of Pathology and Immunology, Faculty of Medicine, University of Geneva

K

Katayoun Falamaki

P

Pratyaksha Wirapati

B

Benedetta Fiordi

I

Isis Senoner

D

Daniela Claudia Maresca

N

Neil Kallal

D

Danaé Guedj

M

Mario Kreutzfeldt

J

Jean-Christophe Tille

M

Marine M. Leblond

K

Katarzyna Michaud

S

Silvia Pesce

S

Simona Candiani

K

Korneliusz Golebski

J

Julien Dagher

M

Melinda Charrier

C

Caroline Pressacco Brossier

E

Elisabeth Grobet-Jeandin

R

Romina Marone

S

Stéphanie Hugues

L

Lukas T. Jeker

G

Grégory Verdeil

D

Doron Merkler

Department of Pathology and Immunology, Faculty of Medicine, University of Geneva

E

Emanuela Marcenaro

C

Christoph Scheiermann

M

Mohammed Attaleb

D

Daniel Benamran

P

Petros Tsantoulis

G

Giuseppe Ercolano

S

Sara Trabanelli

C

Camilla Jandus