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Article ; Online: Immunogenetic Diversity and Cancer Immunotherapy Disparities.

de Miranda, Noel F C C / Scheeren, Ferenc A

2024 Volume 14, Issue 4, Page(s) 585–588

Abstract: Summary: The success of checkpoint blockade cancer immunotherapies has unequivocally confirmed the critical role of T cells in cancer immunity and boosted the development of immunotherapeutic strategies targeting specific antigens on cancer cells. The ... ...

Abstract	Summary: The success of checkpoint blockade cancer immunotherapies has unequivocally confirmed the critical role of T cells in cancer immunity and boosted the development of immunotherapeutic strategies targeting specific antigens on cancer cells. The vast immunogenetic diversity of human leukocyte antigen (HLA) class I alleles across populations is a key factor influencing the advancement of HLA class I-restricted therapies and related research and diagnostic tools.
MeSH term(s)	Humans ; Immunogenetics ; Neoplasms/genetics ; Neoplasms/therapy ; T-Lymphocytes ; Immunotherapy ; Histocompatibility Antigens Class I
Chemical Substances	Histocompatibility Antigens Class I
Language	English
Publishing date	2024-04-05
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-23-1536
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Zs.A 6916: Show issues

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Article ; Online: Design and Synthesis of DNA Origami Nanostructures to Control TNF Receptor Activation.

Aba, Göktuğ / Scheeren, Ferenc A / Sharp, Thomas H

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2800, Page(s) 35–53

Abstract: Clustering of type II tumor necrosis factor (TNF) receptors (TNFRs) is essential for their activation, yet currently available drugs fail to activate signaling. Some strategies aim to cluster TNFR by using multivalent streptavidin or scaffolds based on ... ...

Abstract	Clustering of type II tumor necrosis factor (TNF) receptors (TNFRs) is essential for their activation, yet currently available drugs fail to activate signaling. Some strategies aim to cluster TNFR by using multivalent streptavidin or scaffolds based on dextran or graphene. However, these strategies do not allow for control of the valency or spatial organization of the ligands, and consequently control of the TNFR activation is not optimal. DNA origami nanostructures allow nanometer-precise control of the spatial organization of molecules and complexes, with defined spacing, number and valency. Here, we demonstrate the design and characterization of a DNA origami nanostructure that can be decorated with engineered single-chain TNF-related apoptosis-inducing ligand (SC-TRAIL) complexes, which show increased cell killing compared to SC-TRAIL alone on Jurkat cells. The information in this chapter can be used as a basis to decorate DNA origami nanostructures with various proteins, complexes, or other biomolecules.
MeSH term(s)	Nanostructures/chemistry ; Humans ; Jurkat Cells ; DNA/chemistry ; DNA/metabolism ; TNF-Related Apoptosis-Inducing Ligand/chemistry ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor/chemistry ; Nanotechnology/methods ; Nucleic Acid Conformation
Chemical Substances	DNA (9007-49-2) ; TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor
Language	English
Publishing date	2024-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3834-7_4
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Article ; Online: Genetic Screening for Novel Regulators of Immune Checkpoint Molecules.

Arens, Ramon / Scheeren, Ferenc A

Trends in immunology

2020 Volume 41, Issue 8, Page(s) 692–705

Abstract: Inhibitory and stimulatory immune checkpoint molecules play important roles in regulating immune responses. An increasing number of these immune regulators are currently being evaluated as targets in putative anti-cancer therapies. Recently, ... ...

Abstract	Inhibitory and stimulatory immune checkpoint molecules play important roles in regulating immune responses. An increasing number of these immune regulators are currently being evaluated as targets in putative anti-cancer therapies. Recently, sophisticated genetic screens have been performed to increase our understanding of immune checkpoint pathways and their immunomodulatory regulators. Here, we summarize novel insights obtained by these screens and discuss new directions to advance possible strategies to treat malignancies.
MeSH term(s)	Genetic Testing ; Humans ; Immune Checkpoint Proteins/genetics ; Immune Checkpoint Proteins/immunology ; Immunotherapy/trends
Chemical Substances	Immune Checkpoint Proteins
Language	English
Publishing date	2020-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2020.06.005
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 2: Show issues

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Article ; Online: CD47/SIRPα axis: bridging innate and adaptive immunity.

van Duijn, Anneloes / Van der Burg, Sjoerd H / Scheeren, Ferenc A

Journal for immunotherapy of cancer

2022 Volume 10, Issue 7

Abstract: Myeloid immune cells are frequently present in the tumor environment, and although they can positively contribute to tumor control they often negatively impact anticancer immune responses. One way of inhibiting the positive contributions of myeloid cells ...

Abstract	Myeloid immune cells are frequently present in the tumor environment, and although they can positively contribute to tumor control they often negatively impact anticancer immune responses. One way of inhibiting the positive contributions of myeloid cells is by signaling through the cluster of differentiation 47 (CD47)/signal regulatory protein alpha (SIRPα) axis. The SIRPα receptor is expressed on myeloid cells and is an inhibitory immune receptor that, upon binding to CD47 protein, delivers a 'don't eat me' signal. As CD47 is often overexpressed on cancer cells, treatments targeting CD47/SIRPα have been under active investigation and are currently being tested in clinical settings. Interestingly, the CD47/SIRPα axis is also involved in T cell-mediated antitumor responses. In this perspective we provide an overview of recent studies showing how therapeutic blockade of the CD47/SIRPα axis improves the adaptive immune response. Furthermore, we discuss the interconnection between the myeloid CD47/SIRPα axis and adaptive T cell responses as well as the potential therapeutic role of the CD47/SIRPα axis in tumors with acquired resistance to the classic immunotherapy through major histocompatibility complex downregulation. Altogether this review provides a profound insight for the optimal exploitation of CD47/SIRPα immune checkpoint therapy.
MeSH term(s)	Adaptive Immunity ; Antigens, Differentiation/metabolism ; Antigens, Differentiation/therapeutic use ; CD47 Antigen/metabolism ; Humans ; Neoplasms/drug therapy ; Phagocytosis
Chemical Substances	Antigens, Differentiation ; CD47 Antigen ; CD47 protein, human
Language	English
Publishing date	2022-07-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-004589
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Article ; Online: Reassessing human MHC-I genetic diversity in T cell studies.

Slieker, Roderick C / Warmerdam, Daniël O / Vermeer, Maarten H / van Doorn, Remco / Heemskerk, Mirjam H M / Scheeren, Ferenc A

Scientific reports

2024 Volume 14, Issue 1, Page(s) 7966

Abstract: The Major Histocompatibility Complex class I (MHC-I) system plays a vital role in immune responses by presenting antigens to T cells. Allele specific technologies, including recombinant MHC-I technologies, have been extensively used in T cell analyses ... ...

Abstract	The Major Histocompatibility Complex class I (MHC-I) system plays a vital role in immune responses by presenting antigens to T cells. Allele specific technologies, including recombinant MHC-I technologies, have been extensively used in T cell analyses for COVID-19 patients and are currently used in the development of immunotherapies for cancer. However, the immense diversity of MHC-I alleles presents challenges. The genetic diversity serves as the foundation of personalized medicine, yet it also poses a potential risk of exacerbating healthcare disparities based on MHC-I alleles. To assess potential biases, we analysed (pre)clinical publications focusing on COVID-19 studies and T cell receptor (TCR)-based clinical trials. Our findings reveal an underrepresentation of MHC-I alleles associated with Asian, Australian, and African descent. Ensuring diverse representation is vital for advancing personalized medicine and global healthcare equity, transcending genetic diversity. Addressing this disparity is essential to unlock the full potential of T cells for enhancing diagnosis and treatment across all individuals.
MeSH term(s)	Humans ; T-Lymphocytes ; Australia ; Histocompatibility Antigens Class I/genetics ; HLA Antigens/genetics ; Genetic Variation ; COVID-19/genetics ; Histocompatibility Antigens Class II/genetics ; Major Histocompatibility Complex ; Alleles
Chemical Substances	Histocompatibility Antigens Class I ; HLA Antigens ; Histocompatibility Antigens Class II
Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-58777-2
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Article ; Online: Inhibition of the Epigenetic Reader BRD4 Reduces SIRPα-Mediated Phagocytosis and Melanoma Invasion.

Scheeren, Ferenc A / van Doorn, Remco

The Journal of investigative dermatology

2021 Volume 141, Issue 2, Page(s) 252–254

Abstract: BRD4 acts as an epigenetic reader to regulate gene transcription. It represents a valid therapeutic target in cancer, and several selective and potent small molecule inhibitors have been discovered. A study by Le et al. (2020) published in Journal of ... ...

Abstract	BRD4 acts as an epigenetic reader to regulate gene transcription. It represents a valid therapeutic target in cancer, and several selective and potent small molecule inhibitors have been discovered. A study by Le et al. (2020) published in Journal of Investigative Dermatology (2020) demonstrates that BRD4 inhibition reduces the invasive behavior of melanoma cells associated with matrix metalloproteinase-2 downregulation and increases phagocytosis by myeloid cells through SIRPα downregulation.
MeSH term(s)	Cell Cycle Proteins/metabolism ; Epigenesis, Genetic ; Humans ; Matrix Metalloproteinase 2 ; Melanoma/genetics ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phagocytosis ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; Nuclear Proteins ; Transcription Factors ; Matrix Metalloproteinase 2 (EC 3.4.24.24)
Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2020.07.023
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Article ; Online: The CD47-SIRPα Immune Checkpoint.

Logtenberg, Meike E W / Scheeren, Ferenc A / Schumacher, Ton N

Immunity

2020 Volume 52, Issue 5, Page(s) 742–752

Abstract: The cytotoxic activity of myeloid cells is regulated by a balance of signals that are transmitted through inhibitory and activating receptors. The Cluster of Differentiation 47 (CD47) protein, expressed on both healthy and cancer cells, plays a pivotal ... ...

Abstract	The cytotoxic activity of myeloid cells is regulated by a balance of signals that are transmitted through inhibitory and activating receptors. The Cluster of Differentiation 47 (CD47) protein, expressed on both healthy and cancer cells, plays a pivotal role in this balance by delivering a "don't eat me signal" upon binding to the Signal-regulatory protein alpha (SIRPα) receptor on myeloid cells. Here, we review the current understanding of the role of the CD47-SIRPα axis in physiological tissue homeostasis and as a promising therapeutic target in, among others, oncology, fibrotic diseases, atherosclerosis, and stem cell therapies. We discuss gaps in understanding and highlight where additional insight will be beneficial to allow optimal exploitation of this myeloid cell checkpoint as a target in human disease.
MeSH term(s)	Animals ; Antigens, Differentiation/immunology ; Antigens, Differentiation/metabolism ; CD47 Antigen/immunology ; CD47 Antigen/metabolism ; Homeostasis/immunology ; Humans ; Immunotherapy ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/therapy ; Protein Binding/immunology ; Receptors, Immunologic/immunology ; Receptors, Immunologic/metabolism ; Signal Transduction/immunology
Chemical Substances	Antigens, Differentiation ; CD47 Antigen ; Receptors, Immunologic ; SIRPA protein, human
Language	English
Publishing date	2020-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2020.04.011
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 69: Show issues

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Article ; Online: CRISPR/Cas9-based Engineering of Immunoglobulin Loci in Hybridoma Cells.

Gall, Camille Le M / Fennemann, Felix L / Van Der Schoot, Johan M S / Scheeren, Ferenc A / Verdoes, Martijn

Bio-protocol

2023 Volume 13, Issue 4, Page(s) e4613

Abstract: Development of the hybridoma technology by Köhler and Milstein (1975) has revolutionized the immunological field by enabling routine use of monoclonal antibodies (mAbs) in research and development efforts, resulting in their successful application in the ...

Abstract	Development of the hybridoma technology by Köhler and Milstein (1975) has revolutionized the immunological field by enabling routine use of monoclonal antibodies (mAbs) in research and development efforts, resulting in their successful application in the clinic today. While recombinant good manufacturing practices production technologies are required to produce clinical grade mAbs, academic laboratories and biotechnology companies still rely on the original hybridoma lines to stably and effortlessly produce high antibody yields at a modest price. In our own work, we were confronted with a major issue when using hybridoma-derived mAbs: there was no control over the antibody format that was produced, a flexibility that recombinant production does allow. We set out to remove this hurdle by genetically engineering antibodies directly in the immunoglobulin (Ig) locus of hybridoma cells. We used clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) and homology-directed repair (HDR) to modify antibody's format [mAb or antigen-binding fragment (Fab')] and isotype. This protocol describes a straightforward approach, with little hands-on time, leading to stable cell lines secreting high levels of engineered antibodies. Parental hybridoma cells are maintained in culture, transfected with a guide RNA (gRNA) targeting the site of interest in the Ig locus and an HDR template to knock in the desired insert and an antibiotic resistance gene. By applying antibiotic pressure, resistant clones are expanded and characterized at the genetic and protein level for their ability to produce modified mAbs instead of the parental protein. Finally, the modified antibody is characterized in functional assays. To demonstrate the versatility of our strategy, we illustrate this protocol with examples where we have (i) exchanged the constant heavy region of the antibody, creating chimeric mAb of a novel isotype, (ii) truncated the antibody to create an antigenic peptide-fused Fab' fragment to produce a dendritic cell-targeted vaccine, and (iii) modified both the constant heavy (CH)1 domain of the heavy chain (HC) and the constant kappa (Cκ) light chain (LC) to introduce site-selective modification tags for further derivatization of the purified protein. Only standard laboratory equipment is required, which facilitates its application across various labs. We hope that this protocol will further disseminate our technology and help other researchers. Graphical abstract.
Language	English
Publishing date	2023-02-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4613
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Article ; Online: Cell-intrinsic TLR2/MyD88 pathway in breast and colon cancer.

Kuo, Angera H / Scheeren, Ferenc A

Cell cycle (Georgetown, Tex.)

2014 Volume 13, Issue 24, Page(s) 3785–3786

MeSH term(s)	Animals ; Breast/pathology ; Breast Neoplasms/pathology ; Carcinogenesis/metabolism ; Colonic Neoplasms/pathology ; Female ; Humans ; Intestinal Mucosa/pathology ; Myeloid Differentiation Factor 88/metabolism ; Toll-Like Receptor 2/metabolism
Chemical Substances	Myeloid Differentiation Factor 88 ; Toll-Like Receptor 2
Language	English
Publishing date	2014-12-05
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/15384101.2014.989947
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Zs.A 5881: Show issues

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Article ; Online: Depletion of Trp53 and Cdkn2a Does Not Promote Self-Renewal in the Mammary Gland but Amplifies Proliferation Induced by TNF-α.

van Weele, Linda J / Scheeren, Ferenc A / Cai, Shang / Kuo, Angera H / Qian, Dalong / Ho, William H D / Clarke, Michael F

Stem cell reports

2021 Volume 16, Issue 2, Page(s) 228–236

Abstract: The mammary epithelium undergoes several rounds of extensive proliferation during the female reproductive cycle. Its expansion is a tightly regulated process, fueled by the mammary stem cells and these cells' unique property of self-renewal. Sufficient ... ...

Abstract	The mammary epithelium undergoes several rounds of extensive proliferation during the female reproductive cycle. Its expansion is a tightly regulated process, fueled by the mammary stem cells and these cells' unique property of self-renewal. Sufficient new cells have to be produced to maintain the integrity of a tissue, but excessive proliferation resulting in tumorigenesis needs to be prevented. Three well-known tumor suppressors, p53, p16
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Cell Proliferation ; Cell Self Renewal ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Epithelial Cells/metabolism ; Female ; Mammary Glands, Animal/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Organoids/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Cdkn2a protein, mouse ; Cyclin-Dependent Kinase Inhibitor p16 ; Tumor Necrosis Factor-alpha ; Tumor Suppressor Protein p53
Language	English
Publishing date	2021-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2020.12.012
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