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Article ; Online: T

Meyran, Deborah / Zhu, Joe Jiang / Butler, Jeanne / Tantalo, Daniela / MacDonald, Sean / Nguyen, Thu Ngoc / Wang, Minyu / Thio, Niko / D'Souza, Criselle / Qin, Vicky Mengfei / Slaney, Clare / Harrison, Aaron / Sek, Kevin / Petrone, Pasquale / Thia, Kevin / Giuffrida, Lauren / Scott, Andrew M / Terry, Rachael L / Tran, Ben /

Desai, Jayesh / Prince, H Miles / Harrison, Simon J / Beavis, Paul A / Kershaw, Michael H / Solomon, Ben / Ekert, Paul G / Trapani, Joseph A / Darcy, Phillip K / Neeson, Paul J

Science translational medicine

2023 Volume 15, Issue 690, Page(s) eabk1900

Abstract: Patients who receive chimeric antigen receptor (CAR)-T cells that are enriched in memory T ... cells exhibit better disease control as a result of increased expansion and persistence of the CAR-T ... cells. Human memory T cells include stem-like CD8 ...

Abstract	Patients who receive chimeric antigen receptor (CAR)-T cells that are enriched in memory T cells exhibit better disease control as a result of increased expansion and persistence of the CAR-T cells. Human memory T cells include stem-like CD8
MeSH term(s)	Humans ; Immunotherapy, Adoptive/methods ; Neoplasms ; T-Lymphocytes ; Cytokines/metabolism ; Stem Cells/metabolism ; Receptors, Antigen, T-Cell/metabolism
Chemical Substances	Cytokines ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abk1900
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Article ; Online: IL-2 targeted to CD8+ T cells promotes robust effector T cell responses and potent antitumor immunity.

Moynihan, Kelly D / Kumar, Manu P / Sultan, Hussein / Pappas, Danielle C / Park, Terrence / Chin, S Michael / Bessette, Paul / Lan, Ruth Y / Nguyen, Henry C / Mathewson, Nathan D / Ni, Irene / Chen, Wei / Lee, Yonghee / Liao-Chan, Sindy / Chen, Jessie / Schumacher, Ton N M / Schreiber, Robert D / Yeung, Yik A / Djuretic, Ivana M

Cancer discovery

2024

Abstract: ... We explored the theory that targeting of IL-2 to CD8+ T cells, which are key anti-tumor effectors ... over 500-fold preference for CD8+ T cells over NK and Treg cells, which may contribute to toxicity and ... immunosuppression, respectively. AB248 recapitulated IL-2's effects on CD8+ T cells in vitro and induced selective ...

Abstract	IL-2 signals pleiotropically on diverse cell types, some of which contribute to therapeutic activity against tumors, while others drive undesired activity, such as immunosuppression or toxicity. We explored the theory that targeting of IL-2 to CD8+ T cells, which are key anti-tumor effectors, could enhance its therapeutic index. To this aim, we developed AB248, CD8 cis-targeted IL-2 that demonstrates over 500-fold preference for CD8+ T cells over NK and Treg cells, which may contribute to toxicity and immunosuppression, respectively. AB248 recapitulated IL-2's effects on CD8+ T cells in vitro and induced selective expansion of CD8+ T cells in primates. In mice, an AB248 surrogate demonstrated superior anti-tumor activity and enhanced tolerability as compared to an untargeted IL-2RBy agonist. Efficacy was associated with expansion and phenotypic enhancement of tumor-infiltrating CD8+ T cells, including the emergence of a "better effector" population. These data support the potential utility of AB248 in clinical settings.
Language	English
Publishing date	2024-04-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-23-1266
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Article ; Online: Bhlhe40 Promotes CD4+ T Helper 1 Cell and Suppresses T Follicular Helper Cell Differentiation during Viral Infection.

Nguyen, Christine / Kudek, Matthew / Zander, Ryan / Niu, Hongshen / Shen, Jian / Bauer, Ashley / Alson, Donia / Khatun, Achia / Chen, Yao / Sun, Jie / Drobyski, William / Edelson, Brian T / Cui, Weiguo

Journal of immunology (Baltimore, Md. : 1950)

2024

Abstract: In response to acute infection, naive CD4+ T cells primarily differentiate into T helper 1 (Th1) or ... T follicular helper (Tfh) cells that play critical roles in orchestrating cellular or humoral arms ... of immunity, respectively. However, despite the well established role of T-bet and BCL-6 in driving Th1 and ...

Abstract	In response to acute infection, naive CD4+ T cells primarily differentiate into T helper 1 (Th1) or T follicular helper (Tfh) cells that play critical roles in orchestrating cellular or humoral arms of immunity, respectively. However, despite the well established role of T-bet and BCL-6 in driving Th1 and Tfh cell lineage commitment, respectively, whether additional transcriptional circuits also underlie the fate bifurcation of Th1 and Tfh cell subsets is not fully understood. In this article, we study how the transcriptional regulator Bhlhe40 dictates the Th1/Tfh differentiation axis in mice. CD4+ T cell-specific deletion of Bhlhe40 abrogates Th1 but augments Tfh differentiation. We also assessed an increase in germinal center B cells and Ab production, suggesting that deletion of Bhlhe40 in CD4+ T cells not only alters Tfh differentiation but also their capacity to provide help to B cells. To identify molecular mechanisms by which Bhlhe40 regulates Th1 versus Tfh lineage choice, we first performed epigenetic profiling in the virus specific Th1 and Tfh cells following LCMV infection, which revealed distinct promoter and enhancer activities between the two helper cell lineages. Furthermore, we identified that Bhlhe40 directly binds to cis-regulatory elements of Th1-related genes such as Tbx21 and Cxcr6 to activate their expression while simultaneously binding to regions of Tfh-related genes such as Bcl6 and Cxcr5 to repress their expression. Collectively, our data suggest that Bhlhe40 functions as a transcription activator to promote Th1 cell differentiation and a transcription repressor to suppress Tfh cell differentiation.
Language	English
Publishing date	2024-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300355
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Article: Disrupting CD38-driven T cell dysfunction restores sensitivity to cancer immunotherapy.

Revach, Or-Yam / Cicerchia, Angelina M / Shorer, Ofir / Petrova, Boryana / Anderson, Seth / Park, Joshua / Chen, Lee / Mehta, Arnav / Wright, Samuel J / McNamee, Niamh / Tal-Mason, Aya / Cattaneo, Giulia / Tiwari, Payal / Xie, Hongyan / Sweere, Johanna M / Cheng, Li-Chun / Sigal, Natalia / Enrico, Elizabeth / Miljkovic, Marisa /

Evans, Shane A / Nguyen, Ngan / Whidden, Mark E / Srinivasan, Ramji / Spitzer, Matthew H / Sun, Yi / Sharova, Tatyana / Lawless, Aleigha R / Michaud, William A / Rasmussen, Martin Q / Fang, Jacy / Palin, Claire A / Chen, Feng / Wang, Xinhui / Ferrone, Cristina R / Lawrence, Donald P / Sullivan, Ryan J / Liu, David / Sachdeva, Uma M / Sen, Debattama R / Flaherty, Keith T / Manguso, Robert T / Bod, Lloyd / Kellis, Manolis / Boland, Genevieve M / Yizhak, Keren / Yang, Jiekun / Kanarek, Naama / Sade-Feldman, Moshe / Hacohen, Nir / Jenkins, Russell W

bioRxiv : the preprint server for biology

2024

Abstract: A central problem in cancer immunotherapy with immune checkpoint blockade (ICB) is the development of resistance, which affects 50% of patients with metastatic ... ...

Abstract	A central problem in cancer immunotherapy with immune checkpoint blockade (ICB) is the development of resistance, which affects 50% of patients with metastatic melanoma
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.12.579184
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Article ; Online: Selective decrease of donor-reactive T

Science translational medicine

2022 Volume 14, Issue 669, Page(s) eabo2628

Abstract: ... drugs that patients need to take, reducing lifetime risks of mortality and morbidity. Regulatory T ... cells (T ...

Abstract	Promoting immune tolerance to transplanted organs can minimize the amount of immunosuppressive drugs that patients need to take, reducing lifetime risks of mortality and morbidity. Regulatory T cells (T
MeSH term(s)	Humans ; Transplantation Tolerance ; Liver Transplantation/methods ; T-Lymphocytes, Regulatory ; Graft Rejection/prevention & control ; Living Donors
Language	English
Publishing date	2022-11-02
Publishing country	United States
Document type	Clinical Trial, Phase II ; Clinical Trial, Phase I ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abo2628
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Zs.A 6941: Show issues

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Article ; Online: Evaluation of T-cell clonality by anti-TRBC1 antibody-based flow cytometry and correlation with T-cell receptor sequencing.

Nguyen, Phillip C / Nguyen, Tamia / Wilson, Clarissa / Tiong, Ing Soo / Baldwin, Kylie / Nguyen, Vuong / Came, Neil / Blombery, Piers / Westerman, David A

British journal of haematology

2023 Volume 204, Issue 3, Page(s) 910–920

Abstract: Flow cytometry (FC) incorporating the T-cell receptor β constant chain-1 (TRBC1) has been recently ... proposed as a new standard in T-cell clonality assessment. While early studies demonstrated high ... sequencing gene panel. Our cohort consisted of 90 evaluable samples from 57 patients. TRBC1-FC confirmed T ...

Abstract	Flow cytometry (FC) incorporating the T-cell receptor β constant chain-1 (TRBC1) has been recently proposed as a new standard in T-cell clonality assessment. While early studies demonstrated high sensitivity in samples with conspicuous tumour burden, performance in real-world samples, including those with low tumour burden and correlation with molecular methods has been limited. We evaluated TRBC1-FC performance and correlated the results with high-throughput TRB sequencing and a targeted next-generation sequencing gene panel. Our cohort consisted of 90 evaluable samples from 57 patients. TRBC1-FC confirmed T-cell clonality in 37 out of 38 samples (97%) that were involved in a mature T-cell neoplasm (MTCN). T-cell clonality was also identified in nine samples from patients lacking a current or prior diagnosis of MTCN, consistent with the emerging entity T-cell clonality of uncertain significance. TRBC-FC was polyclonal in all samples and negative for disease involvement by standard pathology assessment. However, correlation with TRB sequencing in 17 of these samples identified two cases that harboured the known clonal sequence from index testing, indicating the presence of measurable residual disease not otherwise detected. Our study provides real-world correlative validation of TRBC1-FC, highlighting the strengths and limitations pertinent to its increasing implementation by general diagnostic laboratories.
MeSH term(s)	Humans ; T-Lymphocytes/pathology ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Flow Cytometry/methods ; Receptors, Antigen, T-Cell ; Lymphoma/pathology
Chemical Substances	Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-12-14
Publishing country	England
Document type	Journal Article
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.19252
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Article ; Online: Cutting Edge: Optimal Formation of Hepatic Tissue-Resident Memory CD4 T Cells Requires T-bet Regulation of CD18.

Depew, Claire E / Nguyen, Alana T / Franke, Marissa C / Calderon, Jesica / Sciammas, Roger / McSorley, Stephen J

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 211, Issue 2, Page(s) 180–185

Abstract: CD4 tissue-resident memory T cells (TRMs) allow robust protection of barrier surfaces against ... pathogens. We investigated the role of T-bet in the formation of liver CD4 TRMs using mouse models. T-bet ... deficient CD4 T cells did not efficiently form liver TRMs when compared with wild-type (WT). In addition ...

Abstract	CD4 tissue-resident memory T cells (TRMs) allow robust protection of barrier surfaces against pathogens. We investigated the role of T-bet in the formation of liver CD4 TRMs using mouse models. T-bet-deficient CD4 T cells did not efficiently form liver TRMs when compared with wild-type (WT). In addition, ectopic expression of T-bet enhanced the formation of liver CD4 TRMs, but only when in competition with WT CD4 T cells. Liver TRMs also expressed higher levels of CD18, which was T-bet dependent. The WT competitive advantage was blocked by Ab neutralization of CD18. Taken together, our data show that activated CD4 T cells compete for entry to liver niches via T-bet-induced expression of CD18, allowing TRM precursors to access subsequent hepatic maturation signals. These findings uncover an essential role for T-bet in liver TRM CD4 formation and suggest targeted enhancement of this pathway could increase the efficacy of vaccines that require hepatic TRMs.
MeSH term(s)	Animals ; Mice ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; Immunologic Memory ; Liver ; Memory T Cells ; CD18 Antigens
Chemical Substances	CD18 Antigens
Language	English
Publishing date	2023-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300017
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Article ; Online: Framework for in vivo T cell screens.

Milling, Lauren E / Markson, Samuel C / Tjokrosurjo, Qin / Derosia, Nicole M / Streeter, Ivy S L / Hickok, Grant H / Lemmen, Ashlyn M / Nguyen, Thao H / Prathima, Priyamvada / Fithian, William / Schwartz, Marc A / Hacohen, Nir / Doench, John G / LaFleur, Martin W / Sharpe, Arlene H

The Journal of experimental medicine

2024 Volume 221, Issue 4

Abstract: In vivo T cell screens are a powerful tool for elucidating complex mechanisms of immunity ... gene library size, cell transfer quantity, and number of mice. Here, we describe the Framework for In vivo T ... for diverse in vivo contexts. As a proof-of-concept, we used FITS to optimize the parameters for a CD8+ T cell ...

Abstract	In vivo T cell screens are a powerful tool for elucidating complex mechanisms of immunity, yet there is a lack of consensus on the screen design parameters required for robust in vivo screens: gene library size, cell transfer quantity, and number of mice. Here, we describe the Framework for In vivo T cell Screens (FITS) to provide experimental and analytical guidelines to determine optimal parameters for diverse in vivo contexts. As a proof-of-concept, we used FITS to optimize the parameters for a CD8+ T cell screen in the B16-OVA tumor model. We also included unique molecular identifiers (UMIs) in our screens to (1) improve statistical power and (2) track T cell clonal dynamics for distinct gene knockouts (KOs) across multiple tissues. These findings provide an experimental and analytical framework for performing in vivo screens in immune cells and illustrate a case study for in vivo T cell screens with UMIs.
MeSH term(s)	Animals ; Mice ; CD8-Positive T-Lymphocytes ; Gene Knockout Techniques
Language	English
Publishing date	2024-02-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230699
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Article ; Online: Mechanics of leukemic T-cell.

Bui, Van-Chien / Nguyen, Thi-Huong

Journal of molecular recognition : JMR

2023 Volume 36, Issue 7, Page(s) e3019

Abstract: ... leukemic T-cells in both interphase and mitotic phases. We found that the elasticity of an individual cell ...

Abstract	Cell mechanics is a factor that determines cell growth, migration, proliferation, or differentiation, as well as trafficking inside the cytoplasm and organization of organelles. Knowledge about cell mechanics is critical to gaining insight into these biological processes. Here, we used atomic force microscopy to examine the elasticity, an important parameter of cell mechanics, of non-adherent Jurkat leukemic T-cells in both interphase and mitotic phases. We found that the elasticity of an individual cell does not significantly change at interphase. When a cell starts to divide, its elasticity increases in the transition from metaphase to telophase during normal division while the cell is stiffened right after it enters mitosis during abnormal division. At the end of the division, the cell elasticity gradually returned to the value of the mother cell. These changes may originate from the changes in cell surface tension during modulating actomyosin at the cleavage furrow, redistributing cell organelles, and constricting the contractile ring to sever mother cell to form daughters. The difference in elasticity patterns suggests that there is a discrepancy in the redistribution of the cell organelles during normal and abnormal division.
MeSH term(s)	Mitosis ; Cell Cycle ; Telophase ; Interphase ; T-Lymphocytes
Language	English
Publishing date	2023-05-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1015084-5
ISSN	1099-1352 ; 0952-3499
ISSN (online)	1099-1352
ISSN	0952-3499
DOI	10.1002/jmr.3019
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Article ; Online: Circulating T

Science translational medicine

2018 Volume 10, Issue 428

Abstract: ... to combat seasonal influenza infections. IIV activates B cells and T follicular helper (T ...

Abstract	Immunization with the inactivated influenza vaccine (IIV) remains the most effective strategy to combat seasonal influenza infections. IIV activates B cells and T follicular helper (T
MeSH term(s)	Adult ; Antibodies, Viral/immunology ; Antibody-Producing Cells/metabolism ; Antigens, CD/metabolism ; B-Lymphocytes/immunology ; Hemagglutinin Glycoproteins, Influenza Virus/metabolism ; Humans ; Immunity, Cellular ; Immunologic Memory ; Influenza, Human/blood ; Influenza, Human/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Vaccination ; Vaccines, Inactivated/immunology
Chemical Substances	Antibodies, Viral ; Antigens, CD ; Hemagglutinin Glycoproteins, Influenza Virus ; Vaccines, Inactivated
Language	English
Publishing date	2018-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.aan8405
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