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  1. Article ; Online: Learning while treating: Gain-of-function STAT6 variants in severe allergic disease.

    Smith, Tukisa D / Doherty, Taylor A

    Cell reports. Medicine

    2023  Volume 4, Issue 5, Page(s) 101040

    Abstract: In an era of rapid identification of inborn errors of immunity, Sharma et al. ...

    Abstract In an era of rapid identification of inborn errors of immunity, Sharma et al.
    MeSH term(s) Humans ; STAT6 Transcription Factor/genetics ; Trans-Activators/genetics ; Gain of Function Mutation ; Hypersensitivity/genetics ; Hypersensitivity/therapy
    Chemical Substances STAT6 Transcription Factor ; Trans-Activators ; STAT6 protein, human
    Language English
    Publishing date 2023-05-17
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Comment
    ISSN 2666-3791
    ISSN (online) 2666-3791
    DOI 10.1016/j.xcrm.2023.101040
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  2. Article ; Online: Intravenous saline may not be a placebo in patients with small fiber neuropathy.

    Blitshteyn, Svetlana / Doherty, Taylor A

    Muscle & nerve

    2023  Volume 67, Issue 6, Page(s) E25–E26

    MeSH term(s) Humans ; Small Fiber Neuropathy/drug therapy ; Saline Solution/administration & dosage ; Administration, Intravenous
    Chemical Substances Saline Solution
    Language English
    Publishing date 2023-04-12
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 438353-9
    ISSN 1097-4598 ; 0148-639X
    ISSN (online) 1097-4598
    ISSN 0148-639X
    DOI 10.1002/mus.27826
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    Zs.A 1449: Show issues Location:
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  3. Article ; Online: Detection, Isolation, and Functional Studies of Mouse Pulmonary Group 2 Innate Lymphoid Cells.

    Strohm, Allyssa N / Doherty, Taylor A

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

    2022  Volume 2506, Page(s) 167–186

    Abstract: ILC2s are key players in the emergence of type 2 inflammation in many pulmonary diseases. While several phenotypic markers can be used to identify ILC2s, our method utilizes the surface markers CD127 and ST2 to classify a group of type 2 cytokine- ... ...

    Abstract ILC2s are key players in the emergence of type 2 inflammation in many pulmonary diseases. While several phenotypic markers can be used to identify ILC2s, our method utilizes the surface markers CD127 and ST2 to classify a group of type 2 cytokine-producing ILC2s upon activation by the fungal allergen Alternaria alternata . Here, we provide our protocol for the detection and isolation of a highly pure population of pulmonary mouse ILCs via flow cytometry and cell sorting. We also describe the methods for in vitro stimulation to assess the functionality of ILC2s.
    MeSH term(s) Animals ; Cytokines ; Immunity, Innate ; Inflammation ; Lung ; Lymphocytes ; Mice
    Chemical Substances Cytokines
    Language English
    Publishing date 2022-06-30
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2364-0_12
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  4. Article ; Online: Insights into the biology of IL-9 in asthma.

    Doherty, Taylor A / Broide, David H

    The Journal of allergy and clinical immunology

    2022  Volume 150, Issue 3, Page(s) 585–586

    MeSH term(s) Arginase ; Asthma ; Biology ; Humans ; Interleukin-13 ; Interleukin-9
    Chemical Substances Interleukin-13 ; Interleukin-9 ; Arginase (EC 3.5.3.1)
    Language English
    Publishing date 2022-06-02
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    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.2022.05.015
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  5. Article ; Online: Military burn pit exposure and airway disease: Implications for our Veteran population.

    Wang, Xinyu / Doherty, Taylor A / James, Christine

    Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology

    2023  Volume 131, Issue 6, Page(s) 720–725

    Abstract: Millions of veterans have been exposed to burn pit smoke during combat deployments throughout the last three decades. Toxic compounds present in burn pit fumes that may cause or exacerbate upper and lower airway diseases include dioxins, polyaromatic ... ...

    Abstract Millions of veterans have been exposed to burn pit smoke during combat deployments throughout the last three decades. Toxic compounds present in burn pit fumes that may cause or exacerbate upper and lower airway diseases include dioxins, polyaromatic hydrocarbons, and particulate matter, among others. There have been several observational studies evaluating the potential role of burn pit exposure in the development of a multitude chronic health conditions, and the veterans Administration has established the Airborne Hazards and Open Burn Pit Registry in 2014. However, specific causality of airway disease from burn pits has been difficult to prove, and there are multiple barriers toward etiologic research. Preclinical models have demonstrated airway dysfunction and inflammation but modeling human exposures remains challenging. Here, we review the current literature on the potential impact of burn pit exposure on chronic airway disease.
    MeSH term(s) Humans ; Veterans ; Incineration ; Occupational Exposure/adverse effects ; Military Personnel ; Pulmonary Disease, Chronic Obstructive/epidemiology ; Chronic Disease
    Language English
    Publishing date 2023-06-19
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1228189-x
    ISSN 1534-4436 ; 0003-4738 ; 1081-1206
    ISSN (online) 1534-4436
    ISSN 0003-4738 ; 1081-1206
    DOI 10.1016/j.anai.2023.06.012
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  6. Article ; Online: Monitoring Group 2 Innate Lymphoid Cell Biology in Models of Lung Inflammation.

    Badrani, Jana H / Strohm, Allyssa N / Haung, Yung-An / Doherty, Taylor A

    Bio-protocol

    2023  Volume 13, Issue 14, Page(s) e4717

    Abstract: Innate lymphoid cells (ILCs) are a rare cell population subdivided into ILC1s, ILC2s, and ILC3s, based on transcription factor expression and cytokine production. In models of lung inflammation, the release of alarmins from the epithelium activates ILC2s ...

    Abstract Innate lymphoid cells (ILCs) are a rare cell population subdivided into ILC1s, ILC2s, and ILC3s, based on transcription factor expression and cytokine production. In models of lung inflammation, the release of alarmins from the epithelium activates ILC2s and promotes the production of Th2-cytokines and the proliferation and migration of ILC2s within the lung. ILC2s are the innate counterpart to CD4
    Language English
    Publishing date 2023-07-20
    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.4717
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  7. Article ; Online: Cellular interactions in aspirin-exacerbated respiratory disease.

    Badrani, Jana H / Doherty, Taylor A

    Current opinion in allergy and clinical immunology

    2020  Volume 21, Issue 1, Page(s) 65–70

    Abstract: Purpose of review: The purpose of this review is to summarize the complex cellular interactions of aspirin-exacerbated respiratory disease (AERD) and how these interactions promote pathogenic mechanisms of AERD.: Recent findings: In addition to ... ...

    Abstract Purpose of review: The purpose of this review is to summarize the complex cellular interactions of aspirin-exacerbated respiratory disease (AERD) and how these interactions promote pathogenic mechanisms of AERD.
    Recent findings: In addition to characteristic changes in eicosanoid levels, recent studies have identified increases in alarmin cytokines (IL-33, thymic stromal lymphopoietin) as well as activated innate lymphoid and plasma cell populations in samples from AERD patients.
    Summary: Patients with AERD typically demonstrate high levels of proinflammatory eicosanoids including cysteinyl leukotrienes (CysLTs) and prostaglandin D2 (PGD2) and hyporesponsiveness to prostaglandin E2 (PGE2). CysLTs are released by mast cells, eosinophils, and adherent platelets and promote epithelial release of IL-33, which activates mast cells and group 2 innate lymphoid cells (ILC2s) in concert with CysLTs. TSLP induces PGD2 release from mast cells which activates and recruits eosinophils, basophils, Th2 cells, and ILC2s via CRTH2. In turn, ILC2s and other cell types produce Th2 cytokines IL-4, IL-5, and IL-13 that, along with CysLTs and PGD2, promote bronchoconstriction, eosinophilic tissue inflammation, and mucus production.
    MeSH term(s) Aspirin/adverse effects ; Asthma, Aspirin-Induced/blood ; Asthma, Aspirin-Induced/immunology ; Asthma, Aspirin-Induced/pathology ; Basophils/immunology ; Basophils/metabolism ; Bronchoconstriction/drug effects ; Bronchoconstriction/immunology ; Cell Communication/drug effects ; Cytokines/blood ; Cytokines/metabolism ; Eicosanoids/blood ; Eicosanoids/metabolism ; Eosinophilia/blood ; Eosinophilia/chemically induced ; Eosinophilia/immunology ; Humans ; Immunity, Innate/drug effects ; Interleukin-33/blood ; Interleukin-33/metabolism ; Mast Cells/immunology ; Mast Cells/metabolism ; Plasma Cells/immunology ; Plasma Cells/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/immunology ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Th2 Cells/immunology ; Th2 Cells/metabolism
    Chemical Substances Cytokines ; Eicosanoids ; IL33 protein, human ; Interleukin-33 ; TSLP protein, human ; Aspirin (R16CO5Y76E)
    Language English
    Publishing date 2020-12-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2088710-3
    ISSN 1473-6322 ; 1528-4050
    ISSN (online) 1473-6322
    ISSN 1528-4050
    DOI 10.1097/ACI.0000000000000712
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    Zs.A 5666: Show issues Location:
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  8. Article ; Online: Lipid-mediated innate lymphoid cell recruitment and activation in aspirin-exacerbated respiratory disease.

    Cavagnero, Kellen J / Doherty, Taylor A

    Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology

    2020  Volume 126, Issue 2, Page(s) 135–142

    Abstract: Objective: To synthesize investigations into the role of lipid-mediated recruitment and activation of group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease (AERD).: Data sources: A comprehensive literature review of reports ...

    Abstract Objective: To synthesize investigations into the role of lipid-mediated recruitment and activation of group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease (AERD).
    Data sources: A comprehensive literature review of reports pertaining to cellular mechanisms, cytokine, and lipid mediators in AERD, as well as ILC2 activation and recruitment, was performed using PubMed and Google Scholar.
    Study selections: Selections of studies were based on reports of lipid mediators in AERD, cytokine mediators in AERD, type 2 effector cells in AERD, platelets in AERD, AERD treatment, ILC2s in allergic airway disease, and ILC2 activation, inhibition, and trafficking.
    Results: The precise mechanisms of AERD pathogenesis are not well understood. Greater levels of proinflammatory lipid mediators and type 2 cytokines are found in tissues derived from patients with AERD relative to controls. After pathognomonic cyclooxygenase-1 inhibitor reactions, proinflammatory mediator concentrations (prostaglandin D2 and cysteinyl leukotrienes) are rapidly increased, as are ILC2 levels in the nasal mucosa. The ILC2s, which potently generate type 2 cytokines in response to lipid mediator stimulation, may play a key role in AERD pathogenesis.
    Conclusion: Although the literature suggests that lipid-mediated ILC2 activation may occur in AERD, there is a dearth of definitive evidence. Future investigations leveraging novel next-generation single-cell sequencing approaches along with recently developed AERD murine models will better define lipid mediator-induced ILC2 trafficking in patients with AERD.
    MeSH term(s) Animals ; Asthma, Aspirin-Induced/immunology ; Humans ; Immunity, Innate ; Inflammation Mediators/immunology ; Lipids/immunology ; Lymphocytes/immunology
    Chemical Substances Inflammation Mediators ; Lipids
    Language English
    Publishing date 2020-09-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1228189-x
    ISSN 1534-4436 ; 0003-4738 ; 1081-1206
    ISSN (online) 1534-4436
    ISSN 0003-4738 ; 1081-1206
    DOI 10.1016/j.anai.2020.09.011
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  9. Article ; Online: ILC2s: Are they what we think they are?

    Cavagnero, Kellen J / Doherty, Taylor A

    The Journal of allergy and clinical immunology

    2020  Volume 146, Issue 2, Page(s) 280–282

    MeSH term(s) Asthma ; Biomarkers ; Cytokines ; Humans ; Immunity, Innate ; Lymphocytes
    Chemical Substances Biomarkers ; Cytokines
    Language English
    Publishing date 2020-06-12
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    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.2020.05.042
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  10. Article ; Online: Hop to It: The First Animal Model of Autoimmune Postural Orthostatic Tachycardia Syndrome.

    Miller, Amanda J / Doherty, Taylor A

    Journal of the American Heart Association

    2019  Volume 8, Issue 19, Page(s) e014084

    Abstract: See Article Li et al. ...

    Abstract See Article Li et al.
    MeSH term(s) Adrenergic Agents ; Animals ; Disease Models, Animal ; Postural Orthostatic Tachycardia Syndrome ; Rabbits
    Chemical Substances Adrenergic Agents
    Language English
    Publishing date 2019-09-24
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.119.014084
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