SHP2 Targets ITK Downstream of PD-1 to Inhibit T Cell Function.


Journal

Inflammation
ISSN: 1573-2576
Titre abrégé: Inflammation
Pays: United States
ID NLM: 7600105

Informations de publication

Date de publication:
Aug 2021
Historique:
received: 30 11 2020
accepted: 08 02 2021
revised: 28 01 2021
pubmed: 25 2 2021
medline: 24 12 2021
entrez: 24 2 2021
Statut: ppublish

Résumé

PD-1 is a critical therapeutic target in cancer immunotherapy and antibodies blocking PD-1 are approved for multiple types of malignancies. The phosphatase SHP2 is the main effector mediating PD-1 downstream signaling and accordingly attempts have been made to target this enzyme as an alternative approach to treat immunogenic tumors. Unfortunately, small molecule inhibitors of SHP2 do not work as expected, suggesting that the role of SHP2 in T cells is more complex than initially hypothesized. To better understand the perplexing role of SHP2 in T cells, we performed interactome mapping of SAP, an adapter protein that is associated with SHP2 downstream signaling. Using genetic and pharmacological approaches, we discovered that SHP2 dephosphorylates ITK specifically downstream of PD-1 and that this event was associated with PD-1 inhibitory cellular functions. This study suggests that ITK is a unique target in this pathway, and since ITK is a SHP2-dependent specific mediator of PD-1 signaling, the combination of ITK inhibitors with PD-1 blockade may improve upon PD-1 monotherapy in the treatment of cancer.

Identifiants

pubmed: 33624224
doi: 10.1007/s10753-021-01437-8
pii: 10.1007/s10753-021-01437-8
pmc: PMC9199348
mid: NIHMS1696709
doi:

Substances chimiques

PDCD1 protein, human 0
Piperidines 0
Programmed Cell Death 1 Receptor 0
Pyrimidines 0
SHP099 0
Protein-Tyrosine Kinases EC 2.7.10.1
emt protein-tyrosine kinase EC 2.7.10.2
PTPN11 protein, human EC 3.1.3.48
Protein Tyrosine Phosphatase, Non-Receptor Type 11 EC 3.1.3.48

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1529-1539

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI125640
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA231277
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI150597
Pays : United States
Organisme : NIH HHS
ID : AI125640
Pays : United States
Organisme : National Institutes of Health (US)
ID : AI150597
Organisme : National Institutes of Health (US)
ID : CA231277
Organisme : NIH HHS
ID : AI125640
Pays : United States
Organisme : Cancer Research Institute
ID : N/A
Pays : United States

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.

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Auteurs

Marianne Strazza (M)

Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, 10032, USA.

Kieran Adam (K)

Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, 10032, USA.

Shalom Lerrer (S)

Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, 10032, USA.

Johanna Straube (J)

Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, 10032, USA.

Sabina Sandigursky (S)

Perlmutter Cancer Center, New York University School of Medicine, New York, NY, 10016, USA.

Beatrix Ueberheide (B)

Proteomics Laboratory, New York University School of Medicine, New York, NY, 10016, USA.

Adam Mor (A)

Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, 10032, USA. am5121@cumc.columbia.edu.
Division of Rheumatology, Columbia University Medical Center, New York, NY, 10032, USA. am5121@cumc.columbia.edu.

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Classifications MeSH