Human colorectal cancer: upregulation of the adaptor protein Rai in TILs leads to cell dysfunction by sustaining GSK-3 activation and PD-1 expression.

CRC Molecular adaptor PD-1 T cell Tumor microenvironment

Journal

Cancer immunology, immunotherapy : CII
ISSN: 1432-0851
Titre abrégé: Cancer Immunol Immunother
Pays: Germany
ID NLM: 8605732

Informations de publication

Date de publication:
04 Jan 2024
Historique:
received: 21 07 2023
accepted: 12 12 2023
medline: 4 1 2024
pubmed: 4 1 2024
entrez: 4 1 2024
Statut: epublish

Résumé

The immunosuppressive tumor microenvironment (TME) of colorectal cancer (CRC) is a major hurdle for immune checkpoint inhibitor-based therapies. Hence characterization of the signaling pathways driving T cell exhaustion within TME is a critical need for the discovery of novel therapeutic targets and the development of effective therapies. We previously showed that (i) the adaptor protein Rai is a negative regulator of T cell receptor signaling and T helper 1 (Th1)/Th17 cell differentiation; and (ii) Rai deficiency is implicated in the hyperactive phenotype of T cells in autoimmune diseases. The expression level of Rai was measured by qRT-PCR in paired peripheral blood T cells and T cells infiltrating tumor tissue and the normal adjacent tissue in CRC patients. The impact of hypoxia-inducible factor (HIF)-1α on Rai expression was evaluated in T cells exposed to hypoxia and by performing chromatin immunoprecipitation assays and RNA interference assays. The mechanism by which upregulation of Rai in T cells promotes T cell exhaustion were evaluated by flow cytometric, qRT-PCR and western blot analyses. We show that Rai is a novel HIF-1α-responsive gene that is upregulated in tumor infiltrating lymphocytes of CRC patients compared to patient-matched circulating T cells. Rai upregulation in T cells promoted Programmed cell Death protein (PD)-1 expression and impaired antigen-dependent degranulation of CD8 Our data identify Rai as a hitherto unknown regulator of the TME-induced exhausted phenotype of human T cells.

Sections du résumé

BACKGROUND BACKGROUND
The immunosuppressive tumor microenvironment (TME) of colorectal cancer (CRC) is a major hurdle for immune checkpoint inhibitor-based therapies. Hence characterization of the signaling pathways driving T cell exhaustion within TME is a critical need for the discovery of novel therapeutic targets and the development of effective therapies. We previously showed that (i) the adaptor protein Rai is a negative regulator of T cell receptor signaling and T helper 1 (Th1)/Th17 cell differentiation; and (ii) Rai deficiency is implicated in the hyperactive phenotype of T cells in autoimmune diseases.
METHODS METHODS
The expression level of Rai was measured by qRT-PCR in paired peripheral blood T cells and T cells infiltrating tumor tissue and the normal adjacent tissue in CRC patients. The impact of hypoxia-inducible factor (HIF)-1α on Rai expression was evaluated in T cells exposed to hypoxia and by performing chromatin immunoprecipitation assays and RNA interference assays. The mechanism by which upregulation of Rai in T cells promotes T cell exhaustion were evaluated by flow cytometric, qRT-PCR and western blot analyses.
RESULTS RESULTS
We show that Rai is a novel HIF-1α-responsive gene that is upregulated in tumor infiltrating lymphocytes of CRC patients compared to patient-matched circulating T cells. Rai upregulation in T cells promoted Programmed cell Death protein (PD)-1 expression and impaired antigen-dependent degranulation of CD8
CONCLUSIONS CONCLUSIONS
Our data identify Rai as a hitherto unknown regulator of the TME-induced exhausted phenotype of human T cells.

Identifiants

pubmed: 38175205
doi: 10.1007/s00262-023-03614-0
pii: 10.1007/s00262-023-03614-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2

Subventions

Organisme : ERC Synergy
ID : ERC 951329
Organisme : Fondazione AIRC per la ricerca sul cancro ETS
ID : IG 2017-ID. 20148

Informations de copyright

© 2023. The Author(s).

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Auteurs

Tommaso Montecchi (T)

Department of Life Sciences, University of Siena, Siena, 53100, Italy.

Giulia Nannini (G)

Department of Experimental and Clinical Medicine, University of Florence, Florence, 50134, Italy.

Domiziana De Tommaso (D)

Department of Life Sciences, University of Siena, Siena, 53100, Italy.

Chiara Cassioli (C)

Department of Life Sciences, University of Siena, Siena, 53100, Italy.

Federica Coppola (F)

Department of Molecular and Developmental Medicine, University of Siena, Siena, 53100, Italy.

Maria Novella Ringressi (MN)

Department of Experimental and Clinical Medicine, University of Florence, Florence, 50134, Italy.

Fabio Carraro (F)

Department of Medical Biotechnologies, University of Siena, Siena, 53100, Italy.

Antonella Naldini (A)

Department of Molecular and Developmental Medicine, University of Siena, Siena, 53100, Italy.

Antonio Taddei (A)

Department of Experimental and Clinical Medicine, University of Florence, Florence, 50134, Italy.

Giuseppe Marotta (G)

Siena University Hospital, Siena, Italy.

Amedeo Amedei (A)

Department of Experimental and Clinical Medicine, University of Florence, Florence, 50134, Italy. amedeo.amedei@unifi.it.

Cosima T Baldari (CT)

Department of Life Sciences, University of Siena, Siena, 53100, Italy. cosima.baldari@unisi.it.

Cristina Ulivieri (C)

Department of Life Sciences, University of Siena, Siena, 53100, Italy. cristina.ulivieri@unisi.it.

Classifications MeSH