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  1. Article ; Online: Identification of IgE as the Allergy-Associated Ig Isotype.

    Finkelman, Fred D

    Journal of immunology (Baltimore, Md. : 1950)

    2017  Volume 198, Issue 1, Page(s) 3–4

    Language English
    Publishing date 2017-01-01
    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.1601893
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    Ud II Zs.37: Show issues Location:
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  2. Article ; Online: Diesel exhaust particle exposure during pregnancy promotes development of asthma and atopy.

    Finkelman, Fred D

    The Journal of allergy and clinical immunology

    2014  Volume 134, Issue 1, Page(s) 73–74

    MeSH term(s) Air Pollutants/toxicity ; Animals ; Asthma/immunology ; Bronchial Hyperreactivity/immunology ; Female ; Humans ; Killer Cells, Natural/immunology ; Pregnancy ; Prenatal Exposure Delayed Effects/immunology ; Vehicle Emissions/toxicity
    Chemical Substances Air Pollutants ; Vehicle Emissions
    Language English
    Publishing date 2014-07
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2014.04.002
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  3. Article ; Online: On sharing unique reagents.

    Finkelman, Fred D

    The Journal of allergy and clinical immunology

    2013  Volume 132, Issue 1, Page(s) 245–246

    MeSH term(s) Animals ; Asthma/etiology ; Disease Models, Animal ; Humans ; Male ; Pyroglyphidae/immunology
    Language English
    Publishing date 2013-07
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2013.02.025
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  4. Article ; Online: The Hdc GC box is critical for Hdc gene transcription and histamine-mediated anaphylaxis.

    Li, Yapeng / Gao, Junfeng / Zhao, Dianzheng / Guan, Xiaoyu / Morris, Suzanne C / Finkelman, Fred D / Huang, Hua

    The Journal of allergy and clinical immunology

    2023  Volume 152, Issue 1, Page(s) 195–204.e3

    Abstract: Background: Histamine is a critical mediator of anaphylaxis, a neurotransmitter, and a regulator of gastric acid secretion. Histidine decarboxylase is a rate-limiting enzyme for histamine synthesis. However, in vivo regulation of Hdc, the gene that ... ...

    Abstract Background: Histamine is a critical mediator of anaphylaxis, a neurotransmitter, and a regulator of gastric acid secretion. Histidine decarboxylase is a rate-limiting enzyme for histamine synthesis. However, in vivo regulation of Hdc, the gene that encodes histidine decarboxylase, is poorly understood.
    Objective: We sought to investigate how enhancers regulate Hdc gene transcription and histamine synthesis in resting conditions and in a mouse model of anaphylaxis.
    Methods: H3K27 acetylation histone modification and chromatin accessibility were used to identify candidate enhancers. The enhancer activity of candidate enhancers was measured in a reporter gene assay, and the function enhancers were validated by CRISPR deletion.
    Results: Deletion of the GC box, which binds to zinc finger transcription factors, in the proximal Hdc enhancer reduced Hdc gene transcription and histamine synthesis in mouse and human mast cell lines. Mast cells, basophils, brain cells, and stomach cells from GC box-deficient mice transcribed the Hdc gene much less than similar cells from wild-type mice, and Hdc GC box-deficient mice failed to develop anaphylaxis.
    Conclusion: The HDC GC box within the proximal enhancer in the mouse and human HDC gene is essential for Hdc gene transcription, histamine synthesis, and histamine-mediated anaphylaxis in vitro and in vivo.
    MeSH term(s) Humans ; Mice ; Animals ; Histidine Decarboxylase/genetics ; Histamine/metabolism ; Anaphylaxis/genetics ; Cell Line ; Transcription, Genetic
    Chemical Substances Histidine Decarboxylase (EC 4.1.1.22) ; Histamine (820484N8I3)
    Language English
    Publishing date 2023-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2023.01.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Microbiota-derived butyrate restricts tuft cell differentiation via histone deacetylase 3 to modulate intestinal type 2 immunity.

    Eshleman, Emily M / Rice, Taylor / Potter, Crystal / Waddell, Amanda / Hashimoto-Hill, Seika / Woo, Vivienne / Field, Sydney / Engleman, Laura / Lim, Hee-Woong / Schumacher, Michael A / Frey, Mark R / Denson, Lee A / Finkelman, Fred D / Alenghat, Theresa

    Immunity

    2024  Volume 57, Issue 2, Page(s) 319–332.e6

    Abstract: Tuft cells in mucosal tissues are key regulators of type 2 immunity. Here, we examined the impact of the microbiota on tuft cell biology in the intestine. Succinate induction of tuft cells and type 2 innate lymphoid cells was elevated with loss of gut ... ...

    Abstract Tuft cells in mucosal tissues are key regulators of type 2 immunity. Here, we examined the impact of the microbiota on tuft cell biology in the intestine. Succinate induction of tuft cells and type 2 innate lymphoid cells was elevated with loss of gut microbiota. Colonization with butyrate-producing bacteria or treatment with butyrate suppressed this effect and reduced intestinal histone deacetylase activity. Epithelial-intrinsic deletion of the epigenetic-modifying enzyme histone deacetylase 3 (HDAC3) inhibited tuft cell expansion in vivo and impaired type 2 immune responses during helminth infection. Butyrate restricted stem cell differentiation into tuft cells, and inhibition of HDAC3 in adult mice and human intestinal organoids blocked tuft cell expansion. Collectively, these data define a HDAC3 mechanism in stem cells for tuft cell differentiation that is dampened by a commensal metabolite, revealing a pathway whereby the microbiota calibrate intestinal type 2 immunity.
    MeSH term(s) Adult ; Mice ; Humans ; Animals ; Intestinal Mucosa ; Tuft Cells ; Butyrates/pharmacology ; Butyrates/metabolism ; Immunity, Innate ; Lymphocytes/metabolism ; Intestines ; Histone Deacetylases/metabolism ; Microbiota ; Cell Differentiation
    Chemical Substances histone deacetylase 3 (EC 3.5.1.98) ; Butyrates ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2024-01-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2024.01.002
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    Zs.A 4227: Show issues Location:
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    Zs.MG 69: Show issues

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  6. Article ; Online: Worming their way into the pharmacy: use of worms and worm products to treat inflammatory diseases.

    Finkelman, Fred D

    Arthritis and rheumatism

    2012  Volume 64, Issue 10, Page(s) 3068–3071

    MeSH term(s) Animals ; Arthritis, Experimental/metabolism ; CD4-Positive T-Lymphocytes/drug effects ; Dendritic Cells/drug effects ; Helminth Proteins/pharmacology ; Interleukin-17/metabolism ; Male
    Chemical Substances ES-62 protein, Acanthocheilonema viteae ; Helminth Proteins ; Interleukin-17
    Language English
    Publishing date 2012-10
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 127294-9
    ISSN 1529-0131 ; 0004-3591 ; 2326-5191
    ISSN (online) 1529-0131
    ISSN 0004-3591 ; 2326-5191
    DOI 10.1002/art.34635
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    Zs.A 24: Show issues Location:
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    Zs.MO 523: Show issues

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  7. Article ; Online: Ezh2-mediated epigenetic modification is required for allogeneic T cell-induced lupus disease.

    Zhen, Yuxuan / Smith, Roger D / Finkelman, Fred D / Shao, Wen-Hai

    Arthritis research & therapy

    2020  Volume 22, Issue 1, Page(s) 133

    Abstract: Background: The mechanisms involved in the pathogenesis of autoimmune disorders, including systemic lupus erythematosus (SLE), have not been fully elucidated. Some of these mechanisms involve epigenetic regulation of gene expression. The histone ... ...

    Abstract Background: The mechanisms involved in the pathogenesis of autoimmune disorders, including systemic lupus erythematosus (SLE), have not been fully elucidated. Some of these mechanisms involve epigenetic regulation of gene expression. The histone methyltransferase Ezh2 contributes to epigenetic regulation of gene expression, is highly expressed in germinal center (GC) B cells and follicular T helper (T
    Methods: The murine bm12 model of lupus-like chronic graft versus host disease (cGVHD) was induced by intra-peritoneal injection of negatively isolated allogeneic CD4
    Results: Decreased autoantibody production and GC formation are observed when Ezh2-deficient CD4
    Conclusion: Ezh2 gene deletion or pharmacological Ezh2 inhibition suppresses autoantibody production and GC formation in bm12 lupus-like cGVHD and decreases affinity maturation and isotype switching in response to immunization with a T cell-dependent antigen. Ezh2 inhibition may be useful for the treatment of lupus and other autoimmune disorders.
    MeSH term(s) Animals ; Epigenesis, Genetic ; Germinal Center ; Graft vs Host Disease/genetics ; Hematopoietic Stem Cell Transplantation ; Lupus Erythematosus, Systemic/genetics ; Mice ; T-Lymphocytes ; T-Lymphocytes, Helper-Inducer
    Language English
    Publishing date 2020-06-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2107602-9
    ISSN 1478-6362 ; 1478-6354
    ISSN (online) 1478-6362
    ISSN 1478-6354
    DOI 10.1186/s13075-020-02225-9
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    Zs.A 5490: Show issues Location:
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  8. Article ; Online: IL-4Rα expression by airway epithelium and smooth muscle accounts for nearly all airway hyperresponsiveness in murine allergic airway disease.

    McKnight, Christopher G / Potter, Crystal / Finkelman, Fred D

    Mucosal immunology

    2019  Volume 13, Issue 2, Page(s) 283–292

    Abstract: Airway hyperresponsiveness (AHR) often defines asthma. Murine allergic airway disease (AAD), like human eosinophilic asthma, is characterized by AHR, eosinophilia, goblet cell metaplasia (GCM), smooth muscle hypercontractility, and increased production ... ...

    Abstract Airway hyperresponsiveness (AHR) often defines asthma. Murine allergic airway disease (AAD), like human eosinophilic asthma, is characterized by AHR, eosinophilia, goblet cell metaplasia (GCM), smooth muscle hypercontractility, and increased production of IL-4 and IL-13-cytokines that induce these characteristics by binding to the IL-4Rα chain. We evaluated the epithelial and smooth muscle IL-4Rα-dependent contributions to AHR of BALB/c mice that possessed 0-2 functional IL-4Rα alleles and had airway disease induced by house dust mite extract (HDM) or exogenous IL-13. Two functional IL-4Rα alleles were required for maximal AHR, while only one functional allele was required for maximal GCM and systemic IL-4/IL-13 levels. Deletion of IL-4Rα from both smooth muscle and epithelial cells inhibited AHR >83% in mice with two functional IL-4Rα alleles. In mice with one functional IL-4Rα allele, selective epithelial cell IL-4Rα deletion maximally inhibited AHR, while selective smooth muscle IL-4Rα deletion decreased IL-13-induced, but not HDM-induced, AHR. Less IL-4Rα signaling is required to maximize the epithelial cell contribution to AHR compared to the smooth muscle contribution to AHR. In addition, epithelial cell responses to IL-4/IL-13 can increase the IL-4Rα-dependent smooth muscle contribution to AHR. These findings carry increasing relevance as IL-4Rα-targeted therapy is administered to human asthmatics.
    MeSH term(s) Animals ; Antigens, Dermatophagoides/immunology ; Cells, Cultured ; Disease Models, Animal ; Female ; Goblet Cells/pathology ; Humans ; Hypersensitivity/immunology ; Interleukin-13/metabolism ; Interleukin-4/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Muscle, Smooth/metabolism ; Pyroglyphidae ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Respiratory Hypersensitivity/immunology ; Respiratory Mucosa/metabolism ; Signal Transduction
    Chemical Substances Antigens, Dermatophagoides ; Il4ra protein, mouse ; Interleukin-13 ; Receptors, Cell Surface ; Interleukin-4 (207137-56-2)
    Language English
    Publishing date 2019-11-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2411370-0
    ISSN 1935-3456 ; 1933-0219
    ISSN (online) 1935-3456
    ISSN 1933-0219
    DOI 10.1038/s41385-019-0232-7
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    Zs.A 6796: Show issues Location:
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  9. Article ; Online: Genetic inhibition of NFATC2 attenuates asparaginase hypersensitivity in mice.

    Rathod, Sanjay / Ramsey, Manda / Finkelman, Fred D / Fernandez, Christian A

    Blood advances

    2020  Volume 4, Issue 18, Page(s) 4406–4416

    Abstract: The family of nuclear factor of activated T cells (NFAT) transcription factors plays a critical role in mediating immune responses. Our previous clinical pharmacogenetic studies suggested that NFATC2 is associated with the risk of hypersensitivity ... ...

    Abstract The family of nuclear factor of activated T cells (NFAT) transcription factors plays a critical role in mediating immune responses. Our previous clinical pharmacogenetic studies suggested that NFATC2 is associated with the risk of hypersensitivity reactions to the chemotherapeutic agent L-asparaginase (ASNase) that worsen outcomes during the treatment of pediatric acute lymphoblastic leukemia. We therefore hypothesized that the genetic inhibition of NFATC2 would protect against the development of anti-ASNase antibodies and ASNase hypersensitivity. Our study demonstrates that ASNase-immunized NFATC2-deficient mice are protected against ASNase hypersensitivity and develop lower antigen-specific and total immunoglobulin E (IgE) levels compared with wild-type (WT) controls. Furthermore, ASNase-immunized NFATC2-deficient mice develop more CD4+ regulatory T cells, fewer CD4+ interleukin-4-positive (IL-4+) cells, higher IL-10/TGF-β1 levels, and lower IL-4/IL-13 levels relative to WT mice. Basophils and peritoneal mast cells from ASNase-immunized, but not naïve, NFATC2-deficient mice had lower FcεRI expression and decreased IgE-mediated mast cell activation than WT mice. Furthermore, ASNase-immunized, but not naïve, NFATC2-deficient mice developed less severe shock than WT mice after induction of passive anaphylaxis or direct histamine administration. Thus, inhibition of NFATC2 protects against ASNase hypersensitivity by impairing T helper 2 responses, which may provide a novel strategy for attenuating hypersensitivity and the development of antidrug antibodies, including to ASNase.
    MeSH term(s) Animals ; Antibodies/therapeutic use ; Antineoplastic Agents/therapeutic use ; Asparaginase/therapeutic use ; Mice ; NFATC Transcription Factors ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Transcription Factors
    Chemical Substances Antibodies ; Antineoplastic Agents ; NFATC Transcription Factors ; Nfatc2 protein, mouse ; Transcription Factors ; Asparaginase (EC 3.5.1.1)
    Language English
    Publishing date 2020-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2020002478
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    Zs.A 7153: Show issues Location:
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  10. Article ; Online: The Akt-mTORC1 pathway mediates Axl receptor tyrosine kinase-induced mesangial cell proliferation.

    Zhen, Yuxuan / McGaha, Tracy L / Finkelman, Fred D / Shao, Wen-Hai

    Journal of leukocyte biology

    2021  Volume 111, Issue 3, Page(s) 563–571

    Abstract: Glomerulonephritis (GN), an important pathologic feature of many renal diseases, is frequently characterized by mesangial cell proliferation. We and others have previously shown that the TAM family receptor tyrosine kinases Axl, Mer, and Tyro-3 ... ...

    Abstract Glomerulonephritis (GN), an important pathologic feature of many renal diseases, is frequently characterized by mesangial cell proliferation. We and others have previously shown that the TAM family receptor tyrosine kinases Axl, Mer, and Tyro-3 contribute to cell survival, proliferation, migration, and clearance of apoptotic cells (ACs); that Axl contributes to GN by promoting mesangial cell proliferation; and that small molecule inhibition of Axl ameliorates nephrotoxic serum-induced GN in mice. We now show that stimulation of renal mesangial cell Axl causes a modest increase in intracellular Ca
    MeSH term(s) Animals ; Cell Proliferation ; Female ; Glomerulonephritis ; Humans ; Intercellular Signaling Peptides and Proteins ; Male ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; NF-kappa B ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-akt ; Receptor Protein-Tyrosine Kinases ; TOR Serine-Threonine Kinases ; c-Mer Tyrosine Kinase
    Chemical Substances Intercellular Signaling Peptides and Proteins ; NF-kappa B ; Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1) ; c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-07-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.2A1220-850RRR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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