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Article ; Online: Critical Functions of IRF4 in B and T Lymphocytes.

Hagman, James

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 11, Page(s) 3715–3716

Language	English
Publishing date	2017-12-01
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.1701385
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Article ; Online: Editorial overview: Lymphocyte development and activation: Lymphoid cell differentiation: choosing paths to traverse the immune landscape.

Hagman, James

Current opinion in immunology

2016 Volume 39, Page(s) v–vii

MeSH term(s)	Animals ; Cell Differentiation/physiology ; Humans ; Lymphocyte Activation/physiology ; Lymphocytes/cytology ; Lymphocytes/physiology ; Stem Cells/cytology
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Editorial
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2016.02.005
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Article ; Online: Conveying the message: identification of Ig-alpha and Ig-beta as components of the B cell receptor complex.

Hagman, James

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 183, Issue 3, Page(s) 1503–1504

MeSH term(s)	CD79 Antigens ; Humans ; Immunoglobulin alpha-Chains ; Receptors, Antigen, B-Cell/chemistry ; Signal Transduction
Chemical Substances	CD79 Antigens ; Immunoglobulin alpha-Chains ; Receptors, Antigen, B-Cell
Language	English
Publishing date	2009-08-01
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.0990055
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Article ; Online: Mi-2β promotes immune evasion in melanoma by activating EZH2 methylation.

Li, Cang / Wang, Zhengyu / Yao, Licheng / Lin, Xingyu / Jian, Yongping / Li, Yujia / Zhang, Jie / Shao, Jingwei / Tran, Phuc D / Hagman, James R / Cao, Meng / Cong, Yusheng / Li, Hong-Yu / Goding, Colin R / Xu, Zhi-Xiang / Liao, Xuebin / Miao, Xiao / Cui, Rutao

Nature communications

2024 Volume 15, Issue 1, Page(s) 2163

Abstract: Recent development of new immune checkpoint inhibitors has been particularly successfully in cancer treatment, but still the majority patients fail to benefit. Converting resistant tumors to immunotherapy sensitive will provide a significant improvement ... ...

Abstract	Recent development of new immune checkpoint inhibitors has been particularly successfully in cancer treatment, but still the majority patients fail to benefit. Converting resistant tumors to immunotherapy sensitive will provide a significant improvement in patient outcome. Here we identify Mi-2β as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Studies in genetically engineered mouse melanoma models indicate that loss of Mi-2β rescues the immune response to immunotherapy in vivo. Mechanistically, ATAC-seq analysis shows that Mi-2β controls the accessibility of IFN-γ-stimulated genes (ISGs). Mi-2β binds to EZH2 and promotes K510 methylation of EZH2, subsequently activating the trimethylation of H3K27 to inhibit the transcription of ISGs. Finally, we develop an Mi-2β-targeted inhibitor, Z36-MP5, which reduces Mi-2β ATPase activity and reactivates ISG transcription. Consequently, Z36-MP5 induces a response to immune checkpoint inhibitors in otherwise resistant melanoma models. Our work provides a potential therapeutic strategy to convert immunotherapy resistant melanomas to sensitive ones.
MeSH term(s)	Animals ; Humans ; Mice ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Immune Evasion/genetics ; Melanoma/drug therapy ; Methylation ; DNA Helicases/genetics ; DNA Helicases/metabolism
Chemical Substances	Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; EZH2 protein, human (EC 2.1.1.43) ; Immune Checkpoint Inhibitors ; Mi-2beta protein, mouse (EC 3.6.1.3) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2024-03-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46422-5
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Article ; Online: Mi-2/NuRD chromatin remodeling complexes regulate B and T-lymphocyte development and function.

Dege, Carissa / Hagman, James

Immunological reviews

2014 Volume 261, Issue 1, Page(s) 126–140

Abstract: Mi-2/nucleosomal remodeling and deacetylase (NuRD) complexes are important epigenetic regulators of chromatin structure and gene expression. Mi-2/NuRD complexes are an assemblage of proteins that combine key epigenetic regulators necessary for (i) ... ...

Abstract	Mi-2/nucleosomal remodeling and deacetylase (NuRD) complexes are important epigenetic regulators of chromatin structure and gene expression. Mi-2/NuRD complexes are an assemblage of proteins that combine key epigenetic regulators necessary for (i) histone deacetylation and demethylation, (ii) binding to methylated DNA, (iii) mobilization of nucleosomes, and (iv) recruitment of additional regulatory proteins. Depending on their context in chromatin, Mi-2/NuRD complexes either activate or repress gene transcription. In this regard, they are important regulators of hematopoiesis and lymphopoiesis. Mi-2/NuRD complexes maintain pools of hematopoietic stem cells. Specifically, components of these complexes control multiple stages of B-cell development by regulating B-cell specific transcription. With one set of components, they inhibit terminal differentiation of germinal center B cells into plasma B cells. They also mediate gene repression together with Blimp-1 during plasma cell differentiation. In cooperation with Ikaros, Mi-2/NuRD complexes also play important roles in T-cell development, including CD4 versus CD8 fate decisions and peripheral T-cell responses. Dysregulation of NuRD during lymphopoiesis promotes leukemogenesis. Here, we review general properties of Mi-2/NuRD complexes and focus on their functions in gene regulation and development of lymphocytes.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Cell Lineage ; Chromatin Assembly and Disassembly ; Epigenesis, Genetic ; Gene Expression Regulation/immunology ; Humans ; Immunity, Cellular ; Lymphocyte Subsets/immunology ; Lymphopoiesis ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/metabolism ; T-Lymphocytes/immunology
Chemical Substances	Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98)
Language	English
Publishing date	2014-08-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12209
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Article ; Online: Chromodomain helicase DNA-binding 4 (CHD4) regulates early B cell identity and V(D)J recombination.

Hagman, James R / Arends, Tessa / Laborda, Curtis / Knapp, Jennifer R / Harmacek, Laura / O'Connor, Brian P

Immunological reviews

2021 Volume 305, Issue 1, Page(s) 29–42

Abstract: B lymphocytes develop from uncommitted precursors into immunoglobulin (antibody)-producing B cells, a major arm of adaptive immunity. Progression of early progenitors to antibody-expressing cells in the bone marrow is orchestrated by the temporal ... ...

Abstract	B lymphocytes develop from uncommitted precursors into immunoglobulin (antibody)-producing B cells, a major arm of adaptive immunity. Progression of early progenitors to antibody-expressing cells in the bone marrow is orchestrated by the temporal regulation of different gene programs at discrete developmental stages. A major question concerns how B cells control the accessibility of these genes to transcription factors. Research has implicated nucleosome remodeling ATPases as mediators of chromatin accessibility. Here, we describe studies of chromodomain helicase DNA-binding 4 (CHD4; also known as Mi-2β) in early B cell development. CHD4 comprises multiple domains that function in nucleosome mobilization and histone binding. CHD4 is a key component of Nucleosome Remodeling and Deacetylase, or NuRD (Mi-2) complexes, which assemble with other proteins that mediate transcriptional repression. We review data demonstrating that CHD4 is necessary for B lineage identity: early B lineage progression, proliferation in response to interleukin-7, responses to DNA damage, and cell survival in vivo. CHD4-NuRD is also required for the Ig heavy-chain repertoire by promoting utilization of distal variable (V
MeSH term(s)	B-Lymphocytes/metabolism ; DNA ; DNA Helicases/genetics ; DNA Helicases/metabolism ; Humans ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/genetics ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/metabolism ; V(D)J Recombination
Chemical Substances	CHD4 protein, human ; DNA (9007-49-2) ; Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2021-12-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13054
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Article ; Online: Plasma cells for hire: prior experience required.

Hagman, James / Lukin, Kara

Immunity

2013 Volume 39, Issue 1, Page(s) 89–91

Abstract: Activation of IgG⁺ memory B cells accounts for much of the antibodies in secondary immune responses. Here, Kometani et al. (2013) demonstrate that reduced amounts of Bach2 in antigen-experienced memory B cells control the robust production of IgG1⁺ ... ...

Abstract	Activation of IgG⁺ memory B cells accounts for much of the antibodies in secondary immune responses. Here, Kometani et al. (2013) demonstrate that reduced amounts of Bach2 in antigen-experienced memory B cells control the robust production of IgG1⁺ plasma cells.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Basic-Leucine Zipper Transcription Factors/immunology ; Cell Differentiation/immunology ; Plasma Cells/immunology
Chemical Substances	Bach2 protein, mouse ; Basic-Leucine Zipper Transcription Factors
Language	English
Publishing date	2013-07-26
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2013.07.009
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Article ; Online: Activation of Aicda gene transcription by Pax5 in plasmacytoma cells.

Dege, Carissa / Hagman, James

Immunologic research

2012 Volume 55, Issue 1-3, Page(s) 155–161

Abstract: Activation-induced deaminase (AID) is an enzyme responsible for somatic hypermutation and immunoglobulin heavy chain class switch recombination. Because AID causes double-stranded breaks in DNA, its expression is highly regulated and is normally ... ...

Abstract	Activation-induced deaminase (AID) is an enzyme responsible for somatic hypermutation and immunoglobulin heavy chain class switch recombination. Because AID causes double-stranded breaks in DNA, its expression is highly regulated and is normally restricted to germinal-center B cells. Dysregulated AID expression can lead to cancer as a result of AID-mediated chromosomal translocations. Many transcription factors including paired box protein 5 (Pax5) have been implicated in regulating the expression of Aicda, the gene encoding AID. In this study, we demonstrate that exogenous expression of Pax5 in a murine plasmacytoma cell line, 558LμM, leads to robust activation of endogenous Aicda transcription. Pax5 is known to initiate transcription through both its N-terminal-paired DNA-binding domain and its C-terminal-activation domain. Through mutational analysis, we demonstrate that Pax5 regulates Aicda transcription through its C-terminal-activation domain. Together, our work describes a novel system that will be useful for determining how Pax5 regulates Aicda transcription.
MeSH term(s)	Animals ; Cell Line ; Cytidine Deaminase/genetics ; Mice ; PAX5 Transcription Factor/genetics ; Plasmacytoma ; Transcription, Genetic
Chemical Substances	PAX5 Transcription Factor ; AICDA (activation-induced cytidine deaminase) (EC 3.5.4.-) ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2012-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1007/s12026-012-8357-8
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Article: Neuroimaging Findings in Patients with

Jiménez de la Peña, Mar / Jiménez de Domingo, Ana / Tirado, Pilar / Calleja-Pérez, Beatriz / Alcaraz, Luis A / Álvarez, Sara / Williams, Jonathan / Hagman, James R / Németh, Andrea H / Fernández-Jaén, Alberto

Molecular syndromology

2021 Volume 12, Issue 3, Page(s) 186–193

Abstract: Early B cell factor 3 (EBF3) is a transcription factor involved in brain development. Heterozygous, loss-of-function mutations ... ...

Abstract	Early B cell factor 3 (EBF3) is a transcription factor involved in brain development. Heterozygous, loss-of-function mutations in
Language	English
Publishing date	2021-04-09
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2546218-0
ISSN	1661-8777 ; 1661-8769
ISSN (online)	1661-8777
ISSN	1661-8769
DOI	10.1159/000513583
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Article ; Online: α1-Antitrypsin Binds to the Glucocorticoid Receptor with Anti-Inflammatory and Antimycobacterial Significance in Macrophages.

Bai, Xiyuan / Bai, An / Tomasicchio, Michele / Hagman, James R / Buckle, Ashley M / Gupta, Arnav / Kadiyala, Vineela / Bevers, Shaun / Serban, Karina A / Kim, Kevin / Feng, Zhihong / Spendier, Kathrin / Hagen, Guy / Fornis, Lorelenn / Griffith, David E / Dzieciatkowska, Monika / Sandhaus, Robert A / Gerber, Anthony N / Chan, Edward D

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 9, Page(s) 1746–1759

Abstract: α1-Antitrypsin (AAT), a serine protease inhibitor, is the third most abundant protein in plasma. Although the best-known function of AAT is irreversible inhibition of elastase, AAT is an acute-phase reactant and is increasingly recognized to have a ... ...

Abstract	α1-Antitrypsin (AAT), a serine protease inhibitor, is the third most abundant protein in plasma. Although the best-known function of AAT is irreversible inhibition of elastase, AAT is an acute-phase reactant and is increasingly recognized to have a panoply of other functions, including as an anti-inflammatory mediator and a host-protective molecule against various pathogens. Although a canonical receptor for AAT has not been identified, AAT can be internalized into the cytoplasm and is known to affect gene regulation. Because AAT has anti-inflammatory properties, we examined whether AAT binds the cytoplasmic glucocorticoid receptor (GR) in human macrophages. We report the finding that AAT binds to GR using several approaches, including coimmunoprecipitation, mass spectrometry, and microscale thermophoresis. We also performed in silico molecular modeling and found that binding between AAT and GR has a plausible stereochemical basis. The significance of this interaction in macrophages is evinced by AAT inhibition of LPS-induced NF-κB activation and IL-8 production as well as AAT induction of angiopoietin-like 4 protein, which are, in part, dependent on GR. Furthermore, this AAT-GR interaction contributes to a host-protective role against mycobacteria in macrophages. In summary, this study identifies a new mechanism for the gene regulation, anti-inflammatory, and host-defense properties of AAT.
MeSH term(s)	Humans ; alpha 1-Antitrypsin/metabolism ; alpha 1-Antitrypsin Deficiency ; Angiopoietins/metabolism ; Angiopoietins/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Interleukin-8/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages/metabolism ; NF-kappa B/metabolism ; Pancreatic Elastase/metabolism ; Receptors, Glucocorticoid/metabolism ; Serine Proteinase Inhibitors
Chemical Substances	alpha 1-Antitrypsin ; Angiopoietins ; Anti-Inflammatory Agents ; Interleukin-8 ; Lipopolysaccharides ; NF-kappa B ; Pancreatic Elastase (EC 3.4.21.36) ; Receptors, Glucocorticoid ; Serine Proteinase Inhibitors ; SERPINA1 protein, human
Language	English
Publishing date	2022-09-26
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.2200227
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