Triple checkpoint blockade of PD-1, Tim-3, and Lag-3 enhances adoptive T cell immunotherapy in a mouse model of ovarian cancer

The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves engineering T cells to specifically target proteins uniquely overexpressed in tumors, thereby controlling tumor growth without toxicity to health...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Proceedings of the National Academy of Sciences - PNAS Ročník 122; číslo 39; s. e2419888122
Hlavní autoři: Alencar, Gabriel F, Mohamed, Asmaa O, Burnett, Madison G, Jean, Samantha St, Nelson, Anders R, Su, Yapeng, Voillet, Valentin, Bates, Breanna M, Rodgers Suarez, Magdalia, Ruskin, Susan L, Trieu, Lam, Lam, Jennifer L, Bekiranov, Stefan, Gottardo, Raphael, Greenberg, Philip D, Anderson, Kristin G
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 30.09.2025
Témata:
ISSN:1091-6490, 1091-6490
On-line přístup:Zjistit podrobnosti o přístupu
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Abstract The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves engineering T cells to specifically target proteins uniquely overexpressed in tumors, thereby controlling tumor growth without toxicity to healthy tissues. Mesothelin (MSLN) contributes to the malignant and invasive phenotype in ovarian cancer and has limited expression in healthy cells, making it a candidate immunotherapy target. Our previous results in a mouse model of ovarian cancer demonstrated that T cells engineered to express a T cell receptor (TCR) targeting MSLN (TCR ) mediated therapeutic activity, delaying tumor growth and prolonging mouse survival. However, inhibitory ligands expressed in the tumor microenvironment (TME) interacted with inhibitory receptors on activated T cells, suppressing antitumor function. We hypothesized combining engineered T cells with checkpoint blockade would enhance T cell function and improve therapeutic efficacy, but administration of monospecific antibodies targeting individual inhibitory pathways had no significant impact on T cell efficacy. By contrast, the combination of PD-1, Tim-3, and Lag-3 blockade with engineered T cells significantly improved T cell function and overall animal survival relative to treatment with antibody alone or TCR with singlet or doublet antibody combinations. Single-cell RNA sequencing revealed TCR T cells treated with the triplet antibody combination increased expression of genes involved in interferon responses and metabolic function, and reduced expression of genes associated with exhaustion. These results suggest that strategies to disrupt multiple inhibitory pathways simultaneously may be necessary for improved adoptive T cell therapy efficacy in patients.
AbstractList The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves engineering T cells to specifically target proteins uniquely overexpressed in tumors, thereby controlling tumor growth without toxicity to healthy tissues. Mesothelin (MSLN) contributes to the malignant and invasive phenotype in ovarian cancer and has limited expression in healthy cells, making it a candidate immunotherapy target. Our previous results in a mouse model of ovarian cancer demonstrated that T cells engineered to express a T cell receptor (TCR) targeting MSLN (TCR ) mediated therapeutic activity, delaying tumor growth and prolonging mouse survival. However, inhibitory ligands expressed in the tumor microenvironment (TME) interacted with inhibitory receptors on activated T cells, suppressing antitumor function. We hypothesized combining engineered T cells with checkpoint blockade would enhance T cell function and improve therapeutic efficacy, but administration of monospecific antibodies targeting individual inhibitory pathways had no significant impact on T cell efficacy. By contrast, the combination of PD-1, Tim-3, and Lag-3 blockade with engineered T cells significantly improved T cell function and overall animal survival relative to treatment with antibody alone or TCR with singlet or doublet antibody combinations. Single-cell RNA sequencing revealed TCR T cells treated with the triplet antibody combination increased expression of genes involved in interferon responses and metabolic function, and reduced expression of genes associated with exhaustion. These results suggest that strategies to disrupt multiple inhibitory pathways simultaneously may be necessary for improved adoptive T cell therapy efficacy in patients.
The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves engineering T cells to specifically target proteins uniquely overexpressed in tumors, thereby controlling tumor growth without toxicity to healthy tissues. Mesothelin (MSLN) contributes to the malignant and invasive phenotype in ovarian cancer and has limited expression in healthy cells, making it a candidate immunotherapy target. Our previous results in a mouse model of ovarian cancer demonstrated that T cells engineered to express a T cell receptor (TCR) targeting MSLN (TCRMSLN) mediated therapeutic activity, delaying tumor growth and prolonging mouse survival. However, inhibitory ligands expressed in the tumor microenvironment (TME) interacted with inhibitory receptors on activated T cells, suppressing antitumor function. We hypothesized combining engineered T cells with checkpoint blockade would enhance T cell function and improve therapeutic efficacy, but administration of monospecific antibodies targeting individual inhibitory pathways had no significant impact on T cell efficacy. By contrast, the combination of PD-1, Tim-3, and Lag-3 blockade with engineered T cells significantly improved T cell function and overall animal survival relative to treatment with antibody alone or TCRMSLN with singlet or doublet antibody combinations. Single-cell RNA sequencing revealed TCRMSLN T cells treated with the triplet antibody combination increased expression of genes involved in interferon responses and metabolic function, and reduced expression of genes associated with exhaustion. These results suggest that strategies to disrupt multiple inhibitory pathways simultaneously may be necessary for improved adoptive T cell therapy efficacy in patients.The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves engineering T cells to specifically target proteins uniquely overexpressed in tumors, thereby controlling tumor growth without toxicity to healthy tissues. Mesothelin (MSLN) contributes to the malignant and invasive phenotype in ovarian cancer and has limited expression in healthy cells, making it a candidate immunotherapy target. Our previous results in a mouse model of ovarian cancer demonstrated that T cells engineered to express a T cell receptor (TCR) targeting MSLN (TCRMSLN) mediated therapeutic activity, delaying tumor growth and prolonging mouse survival. However, inhibitory ligands expressed in the tumor microenvironment (TME) interacted with inhibitory receptors on activated T cells, suppressing antitumor function. We hypothesized combining engineered T cells with checkpoint blockade would enhance T cell function and improve therapeutic efficacy, but administration of monospecific antibodies targeting individual inhibitory pathways had no significant impact on T cell efficacy. By contrast, the combination of PD-1, Tim-3, and Lag-3 blockade with engineered T cells significantly improved T cell function and overall animal survival relative to treatment with antibody alone or TCRMSLN with singlet or doublet antibody combinations. Single-cell RNA sequencing revealed TCRMSLN T cells treated with the triplet antibody combination increased expression of genes involved in interferon responses and metabolic function, and reduced expression of genes associated with exhaustion. These results suggest that strategies to disrupt multiple inhibitory pathways simultaneously may be necessary for improved adoptive T cell therapy efficacy in patients.
Author Jean, Samantha St
Alencar, Gabriel F
Ruskin, Susan L
Lam, Jennifer L
Bates, Breanna M
Bekiranov, Stefan
Rodgers Suarez, Magdalia
Anderson, Kristin G
Trieu, Lam
Su, Yapeng
Burnett, Madison G
Gottardo, Raphael
Voillet, Valentin
Nelson, Anders R
Greenberg, Philip D
Mohamed, Asmaa O
Author_xml – sequence: 1
  givenname: Gabriel F
  surname: Alencar
  fullname: Alencar, Gabriel F
  organization: Department of Microbiology, Immunology and Cancer Biology, and Beirne B. Carter Center for Immunology Research University of Virginia School of Medicine, Charlottesville, VA 22908
– sequence: 2
  givenname: Asmaa O
  surname: Mohamed
  fullname: Mohamed, Asmaa O
  organization: Department of Microbiology, Immunology and Cancer Biology, and Beirne B. Carter Center for Immunology Research University of Virginia School of Medicine, Charlottesville, VA 22908
– sequence: 3
  givenname: Madison G
  orcidid: 0000-0003-4852-3639
  surname: Burnett
  fullname: Burnett, Madison G
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 4
  givenname: Samantha St
  orcidid: 0000-0001-5555-9299
  surname: Jean
  fullname: Jean, Samantha St
  organization: Department of Pathology and Center for Comparative Medicine, University of Virginia, Charlottesville, VA 22908
– sequence: 5
  givenname: Anders R
  surname: Nelson
  fullname: Nelson, Anders R
  organization: Department of Microbiology, Immunology and Cancer Biology, and Beirne B. Carter Center for Immunology Research University of Virginia School of Medicine, Charlottesville, VA 22908
– sequence: 6
  givenname: Yapeng
  surname: Su
  fullname: Su, Yapeng
  organization: Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109
– sequence: 7
  givenname: Valentin
  orcidid: 0000-0002-5751-3881
  surname: Voillet
  fullname: Voillet, Valentin
  organization: Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, WA 98109
– sequence: 8
  givenname: Breanna M
  surname: Bates
  fullname: Bates, Breanna M
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 9
  givenname: Magdalia
  surname: Rodgers Suarez
  fullname: Rodgers Suarez, Magdalia
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 10
  givenname: Susan L
  orcidid: 0009-0005-2699-7296
  surname: Ruskin
  fullname: Ruskin, Susan L
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 11
  givenname: Lam
  surname: Trieu
  fullname: Trieu, Lam
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 12
  givenname: Jennifer L
  surname: Lam
  fullname: Lam, Jennifer L
  organization: Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
– sequence: 13
  givenname: Stefan
  orcidid: 0000-0002-3177-4346
  surname: Bekiranov
  fullname: Bekiranov, Stefan
  organization: Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908
– sequence: 14
  givenname: Raphael
  surname: Gottardo
  fullname: Gottardo, Raphael
  organization: Biomedical Data Science Center, Division of Clinical Research and Innovation, Lausanne University Hospital & University of Lausanne, and Swiss Institute of Bioinformatics, Lausanne 1005, Switzerland
– sequence: 15
  givenname: Philip D
  orcidid: 0000-0003-3812-647X
  surname: Greenberg
  fullname: Greenberg, Philip D
  organization: Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109
– sequence: 16
  givenname: Kristin G
  orcidid: 0000-0001-9263-4438
  surname: Anderson
  fullname: Anderson, Kristin G
  organization: Department of Obstetrics and Gynecology, University of Virginia School of Medicine, Charlottesville, VA 22908
BackLink https://www.ncbi.nlm.nih.gov/pubmed/40982684$$D View this record in MEDLINE/PubMed
BookMark eNpNkLtPwzAYxC1URB8wsyGPDA34lcYZUXlKlWAIc-THF2qa2CFOKnXhb6cVRWK5u-H00-mmaOSDB4QuKbmhJOO3rVfxhgmaSykpYydoQklOk4XIyehfHqNpjJ-EkDyV5AyNBcklW0gxQd9F59oasFmD2bTB-R7rOpiNsoBDhd_uEzrHhWsSPsfKW7xSHwnH4NfKG4hY2dD2bgu4wAbqGrumGXzo19Cpdoedxwo3YYiwVwv1gRi2qnPKY3MAdOfotFJ1hIujz9D740OxfE5Wr08vy7tVYngq-4RmkupU26rS1cJklYBUCi2tlLnlzGrNKBVGCMgymZtFqnOQghPOtciMNCmboetfbtuFrwFiXzYuHhYrD_t9JWcpF5RRyffVq2N10A3Ysu1co7pd-fcZ-wFYCG-l
ContentType Journal Article
DBID CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1073/pnas.2419888122
DatabaseName Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList MEDLINE
MEDLINE - Academic
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod no_fulltext_linktorsrc
Discipline Sciences (General)
EISSN 1091-6490
ExternalDocumentID 40982684
Genre Journal Article
GrantInformation_xml – fundername: Parker Institute for Cancer Immunotherapy (PICI)
  grantid: no number
– fundername: Celgene Corporation | Juno Therapeutics
  grantid: no number
– fundername: HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
  grantid: 5T32AI007496-29
– fundername: HHS | NIH | National Cancer Institute (NCI)
  grantid: CA009657-26A1 CA266737 P30CA044579 CA018029 CA033084
– fundername: Ovarian Cancer Research Alliance (OCRA)
  grantid: Ann and Sol Schreiber Mentored Investigator Training Grant
– fundername: Lonza Houston (Lonza Houston, Inc.)
  grantid: no number
GroupedDBID ---
-DZ
-~X
.55
0R~
123
2FS
2WC
4.4
5RE
5VS
85S
AACGO
AAFWJ
AANCE
ABOCM
ABPLY
ABPPZ
ABTLG
ABZEH
ACGOD
ACIWK
ACNCT
ACPRK
AENEX
AFFNX
AFHIN
AFRAH
ALMA_UNASSIGNED_HOLDINGS
BKOMP
CGR
CS3
CUY
CVF
D0L
DIK
DU5
E3Z
EBS
ECM
EIF
F5P
FRP
GX1
H13
HH5
JLS
JSG
KQ8
L7B
LU7
N9A
NPM
N~3
O9-
OK1
PNE
PQQKQ
R.V
RHI
RNA
RNS
RPM
RXW
SJN
TAE
TN5
UKR
WH7
WOQ
X7M
XSW
Y6R
YKV
YSK
ZCA
~02
~KM
7X8
ID FETCH-LOGICAL-c358t-1781b5bdffbf6c7f4e584b8d889d32dbb2114c44e7789c65b9e843033b47c8c52
IEDL.DBID 7X8
ISICitedReferencesCount 0
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=001589159400001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1091-6490
IngestDate Tue Sep 23 22:54:54 EDT 2025
Fri Oct 10 01:53:16 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 39
Keywords checkpoint blockade
T cell engineering
ovarian cancer
adoptive cell therapy
immunotherapy
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c358t-1781b5bdffbf6c7f4e584b8d889d32dbb2114c44e7789c65b9e843033b47c8c52
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0002-5751-3881
0000-0001-5555-9299
0000-0003-4852-3639
0000-0002-3177-4346
0009-0005-2699-7296
0000-0003-3812-647X
0000-0001-9263-4438
OpenAccessLink https://doi.org/10.1073/pnas.2419888122
PMID 40982684
PQID 3253412183
PQPubID 23479
ParticipantIDs proquest_miscellaneous_3253412183
pubmed_primary_40982684
PublicationCentury 2000
PublicationDate 2025-09-30
PublicationDateYYYYMMDD 2025-09-30
PublicationDate_xml – month: 09
  year: 2025
  text: 2025-09-30
  day: 30
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle Proceedings of the National Academy of Sciences - PNAS
PublicationTitleAlternate Proc Natl Acad Sci U S A
PublicationYear 2025
SSID ssj0009580
Score 2.4911695
Snippet The five-year survival rate for ovarian cancer patients remains below 50%, underscoring the need for innovative therapies. One promising approach involves...
SourceID proquest
pubmed
SourceType Aggregation Database
Index Database
StartPage e2419888122
SubjectTerms Animals
Antigens, CD - genetics
Antigens, CD - immunology
Antigens, CD - metabolism
Cell Line, Tumor
Disease Models, Animal
Female
Hepatitis A Virus Cellular Receptor 2 - antagonists & inhibitors
Hepatitis A Virus Cellular Receptor 2 - immunology
Hepatitis A Virus Cellular Receptor 2 - metabolism
Humans
Immune Checkpoint Inhibitors - pharmacology
Immunotherapy, Adoptive - methods
Lymphocyte Activation Gene 3 Protein
Mesothelin
Mice
Ovarian Neoplasms - genetics
Ovarian Neoplasms - immunology
Ovarian Neoplasms - pathology
Ovarian Neoplasms - therapy
Programmed Cell Death 1 Receptor - antagonists & inhibitors
Programmed Cell Death 1 Receptor - immunology
T-Lymphocytes - immunology
Tumor Microenvironment - immunology
Title Triple checkpoint blockade of PD-1, Tim-3, and Lag-3 enhances adoptive T cell immunotherapy in a mouse model of ovarian cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/40982684
https://www.proquest.com/docview/3253412183
Volume 122
WOSCitedRecordID wos001589159400001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings 1
isFullTextHit
isPrint
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LbxMxELag7YELUNpCKUWDxIFKcZtde9f2CaFCxAGiHIKUWzR-QRTJuyRRJS797R1vNqKXSkhc9rYjr2c8rx1_H2Pv3bByRZSKKx89l7UruVHC8oBYG6wxiug7sgk1HuvZzEz6htu6H6vc-cTOUfvG5R75lSgrcrg5oH9sf_PMGpX_rvYUGo_ZvqBUJo90qZm-B7qrt2gEpuC1NMMdtI8SV23C9SVFL0MVYJGZcx_KL7s4M3r2vyt8zp72GSZ82prEIXsU0gt22J_hNXzogaYvjtjtdJXb7EB6c8u2WaQNWIptS_QBmgiTz7wYACmTiwFg8vANf3IBIf3CThL6ps3OEqaQ2_-wyFdN-gtdf2CRACH3FQJ0bDtZYnNDlTkmcFnA6pj9GH2ZXn_lPR8Dd6LSG14oynEr62O0sXYqykDZi9Vea-NF6a2lYlI6KYNS2ri6siZoSSFSWKmcdlV5wvZSk8IrBhoVChsps_eFRFlgGalwISOJvlR1hafs3W6P52Tv-SswBVrz_O8un7KXW0XN2y0wx5xqVZ3Ra17_w9tn7EmZqXy70Y83bD_SaQ_n7MDdbBbr1dvOkOg5nny_Aw900rM
linkProvider ProQuest
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Triple+checkpoint+blockade+of+PD-1%2C+Tim-3%2C+and+Lag-3+enhances+adoptive+T+cell+immunotherapy+in+a+mouse+model+of+ovarian+cancer&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+-+PNAS&rft.au=Alencar%2C+Gabriel+F&rft.au=Mohamed%2C+Asmaa+O&rft.au=Burnett%2C+Madison+G&rft.au=Jean%2C+Samantha+St&rft.date=2025-09-30&rft.issn=1091-6490&rft.eissn=1091-6490&rft.volume=122&rft.issue=39&rft.spage=e2419888122&rft_id=info:doi/10.1073%2Fpnas.2419888122&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1091-6490&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1091-6490&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1091-6490&client=summon