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  1. Article ; Online: Howard A. Young's 4 Decades in Science: More Than Just Experiments.

    Wahl, Sharon M

    Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

    2022  Volume 42, Issue 12, Page(s) 611–617

    Language English
    Publishing date 2022-08-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1226675-9
    ISSN 1557-7465 ; 1079-9907
    ISSN (online) 1557-7465
    ISSN 1079-9907
    DOI 10.1089/jir.2022.0093
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Memorial: Nancy McCartney-Francis, 1950-2014.

    Wahl, Sharon M

    Journal of leukocyte biology

    2014  Volume 96, Issue 5, Page(s) 667–668

    MeSH term(s) Biology/history ; Famous Persons ; History, 20th Century ; History, 21st Century ; Leukocytes/immunology ; Leukocytes/metabolism
    Language English
    Publishing date 2014-10-30
    Publishing country United States
    Document type Biography ; Historical Article ; Letter
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.4LT0614-301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Harnessing imaging tools to guide immunotherapy trials: summary from the National Cancer Institute Cancer Imaging Steering Committee workshop.

    Shankar, Lalitha K / Schöder, Heiko / Sharon, Elad / Wolchok, Jedd / Knopp, Michael V / Wahl, Richard L / Ellingson, Benjamin M / Hall, Nathan C / Yaffe, Martin J / Towbin, Alexander J / Farwell, Michael D / Pryma, Daniel / Poussaint, Tina Young / Wright, Chadwick L / Schwartz, Lawrence / Harisinghani, Mukesh / Mahmood, Umar / Wu, Anna M / Leung, David /
    de Vries, Elisabeth G E / Tang, Ying / Beach, Gillian / Reeves, Steven A

    The Lancet. Oncology

    2023  Volume 24, Issue 3, Page(s) e133–e143

    Abstract: As the immuno-oncology field continues the rapid growth witnessed over the past decade, optimising patient outcomes requires an evolution in the current response-assessment guidelines for phase 2 and 3 immunotherapy clinical trials and clinical care. ... ...

    Abstract As the immuno-oncology field continues the rapid growth witnessed over the past decade, optimising patient outcomes requires an evolution in the current response-assessment guidelines for phase 2 and 3 immunotherapy clinical trials and clinical care. Additionally, investigational tools-including image analysis of standard-of-care scans (such as CT, magnetic resonance, and PET) with analytics, such as radiomics, functional magnetic resonance agents, and novel molecular-imaging PET agents-offer promising advancements for assessment of immunotherapy. To document current challenges and opportunities and identify next steps in immunotherapy diagnostic imaging, the National Cancer Institute Clinical Imaging Steering Committee convened a meeting with diverse representation among imaging experts and oncologists to generate a comprehensive review of the state of the field.
    MeSH term(s) United States ; Humans ; National Cancer Institute (U.S.) ; Neoplasms ; Immunotherapy ; Image Processing, Computer-Assisted ; Medical Oncology
    Language English
    Publishing date 2023-03-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2049730-1
    ISSN 1474-5488 ; 1470-2045
    ISSN (online) 1474-5488
    ISSN 1470-2045
    DOI 10.1016/S1470-2045(22)00742-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Transforming growth factor-beta: innately bipolar.

    Wahl, Sharon M

    Current opinion in immunology

    2007  Volume 19, Issue 1, Page(s) 55–62

    Abstract: Widely heralded for depressing ongoing immune responses, renewed interest in the proficiency by which transforming growth factor beta (TGF-beta) not only engages but also might drive an over-reactive innate response highlights its bipolar nature. ... ...

    Abstract Widely heralded for depressing ongoing immune responses, renewed interest in the proficiency by which transforming growth factor beta (TGF-beta) not only engages but also might drive an over-reactive innate response highlights its bipolar nature. Although coordination of the development and function of Treg, in addition to direct inhibition of cellular activation, are prominent pathways by which TGF-beta controls adaptive immunity, paradoxically TGF-beta appears instrumental in initiation of host responses to invasion through recruitment and activation of immune cells and persuasion of Th17 lineage commitment. Nevertheless, true to its manic-depressive behavior, new evidence links TGF-beta with depression of innate cells, including NK cells, and by way of a potential bridge between mast cells and Treg. Disruption of the tenuous balance between these opposing actions of TGF-beta underlies immunopathogenicity.
    MeSH term(s) Animals ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; Cell Lineage/immunology ; Humans ; Immunity, Innate ; Inflammation/immunology ; Inflammation/prevention & control ; Transforming Growth Factor beta/physiology
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2007-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2006.11.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Expression of APOBEC family members as regulators of endogenous retroelements and malignant transformation in systemic autoimmunity.

    Mavragani, Clio P / Kirou, Kyriakos A / Nezos, Adrianos / Seshan, Surya / Wild, Teresa / Wahl, Sharon M / Moutsopoulos, Haralampos M / Crow, Mary K

    Clinical immunology (Orlando, Fla.)

    2020  Volume 223, Page(s) 108649

    Abstract: Objective: To explore whether APOBEC family members are involved in the response to inappropriate expression of L1 retroelements in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE), as well as in SS related lymphomagenesis.: ... ...

    Abstract Objective: To explore whether APOBEC family members are involved in the response to inappropriate expression of L1 retroelements in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE), as well as in SS related lymphomagenesis.
    Methods: Minor salivary glands (MSG) and kidney biopsy (KB) specimens were obtained from 41 SS patients (10 with lymphoma) and 23 patients with SLE, respectively. PBMC and sera were also collected from 73 SLE patients. Full-length L1 transcripts, members of the APOBEC and IFN family were quantitated by real time PCR. Type I IFN activity was assessed in lupus plasma by a cell assay.
    Results: APOBEC3A was increased in SS MSG, SLE KB and PBMC and correlated with L1. AID and APOBEC3G were particularly overexpressed in MSG tissues derived from SS lymphoma patients.
    Conclusion: These data reveal a previously unappreciated role of APOBEC family proteins in the pathogenesis of systemic autoimmunity and SS related lymphomagenesis.
    MeSH term(s) Autoimmunity ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytidine Deaminase/genetics ; Cytidine Deaminase/metabolism ; Endogenous Retroviruses/genetics ; Gene Expression Regulation ; Humans ; Interferons/metabolism ; Kidney/physiology ; Leukocytes, Mononuclear/immunology ; Lupus Erythematosus, Systemic/immunology ; Lymphoma/immunology ; Proteins/genetics ; Proteins/metabolism ; Salivary Glands/physiology ; Sjogren's Syndrome/immunology
    Chemical Substances Proteins ; Interferons (9008-11-1) ; AICDA (activation-induced cytidine deaminase) (EC 3.5.4.-) ; APOBEC3A protein, human (EC 3.5.4.5) ; Cytidine Deaminase (EC 3.5.4.5)
    Language English
    Publishing date 2020-12-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2020.108649
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The mouth: a gateway or a trap for HIV?

    Malamud, Daniel / Wahl, Sharon M

    AIDS (London, England)

    2010  Volume 24, Issue 1, Page(s) 5–16

    MeSH term(s) Female ; HIV Infections/transmission ; HIV Infections/virology ; HIV-1 ; Humans ; Male ; Milk, Human/virology ; Mouth Mucosa/virology ; Pregnancy ; Saliva/virology
    Language English
    Publishing date 2010-01-02
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639076-6
    ISSN 1473-5571 ; 0269-9370 ; 1350-2840
    ISSN (online) 1473-5571
    ISSN 0269-9370 ; 1350-2840
    DOI 10.1097/QAD.0b013e328333525f
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Book: Host defense gone awry

    Wahl, Sharon M

    from inflammation to cancer

    (The Anita B. Roberts lecture series)

    2009  

    Abstract: CIT): The Anita B. Roberts Lecture Series This series highlights outstanding research achievements of women scientists at the NIH. The seminar is dedicated to Dr. Anita Roberts and honors her role as an exceptional mentor and scientist. Anita joined ... ...

    Institution National Institutes of Health (U.S.)
    Author's details Sharon Wahl
    Series title The Anita B. Roberts lecture series
    Abstract (CIT): The Anita B. Roberts Lecture Series This series highlights outstanding research achievements of women scientists at the NIH. The seminar is dedicated to Dr. Anita Roberts and honors her role as an exceptional mentor and scientist. Anita joined the NIH in 1976 and spent 30 years at NCI, rising to Chief of the Laboratory of Cell Regulation and Carcinogenesis. She died of gastric cancer in May 2006, leaving a legacy that touched both the professional and personal lives of all who knew her. Her work focused primarily on TGF-beta and its role in the growth of epithelial and lymphoid cells. In 2003, Thomas Scientific's Science Watch listed her among the 50 most-cited scientists during 1982 to 2002, a feature called "Twenty Years of Citation Superstars." Anita was a superstar to many for her mentoring talent and her ability to balance family and work life. Her successful lab was well known for meeting family needs and for providing an environment both intellectually and emotionally enriching. The lecture series in her name serves to highlight the fact that the NIH recognizes the value and necessity of a supportive workplace. For more information, visit http://www1.od.nih.gov/oir/sourcebook/comm-adv/wsa.htm.
    MeSH term(s) Neoplasms/etiology ; Secretory Leukocyte Peptidase Inhibitor/metabolism ; Cell Transformation, Neoplastic ; Inflammation
    Language English
    Publisher National Institutes of Health
    Publishing place Bethesda, Md
    Document type Book
    Note Open-captioned. ; Title from title screen. ; Streaming video (53 min. : sd., col.).
    Database Catalogue of the US National Library of Medicine (NLM)

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  8. Book: IFN-[alpha], villain or hero?

    Wahl, Sharon M

    2008  

    Abstract: CIT): Dr. Wahl's laboratory studies pathways in innate and regulatory immunity and their role in pathogenesis of inflammatory disease, infection and autoimmunity. In addition to her longstanding interests regarding the pro and anti-inflammatory ... ...

    Title variant Interferon alpha, villain or hero? :
    Institution National Institutes of Health (U.S.). / Immunology Interest Group
    Author's details Sharon Wahl ; Immunology Interest Group
    Abstract (CIT): Dr. Wahl's laboratory studies pathways in innate and regulatory immunity and their role in pathogenesis of inflammatory disease, infection and autoimmunity. In addition to her longstanding interests regarding the pro and anti-inflammatory properties of TGF-β, another focus includes host-pathogen interactions and how phagocytic cells can become unwitting hosts to clever pathogens. In its bid for supremacy over its cellular targets, HIV takes host cell molecules as accomplices in enabling binding, entry, and completion of its life cycle. Although the macrophage is an enabler, it also possesses innate antiviral mechanisms, including APOBEC3 family DNA-editing enzymes. Differential expression of these enzymes, which are largely neutralized by HIV, is associated with viral susceptibility, but IFNx regulates APOBEC to render CD4+ targets tougher combatants to HIV in vitro and in AIDS patients. Although pivotal in host defense, too much IFNx can be detrimental, promoting autoimmune disease. How to harness the good and avoid the bad remains the key question.
    MeSH term(s) HIV/immunology ; Host-Pathogen Interactions ; Immunity, Innate ; Interferon-alpha/immunology ; Macrophages/immunology
    Language English
    Publisher National Institutes of Health
    Publishing place Bethesda, Md
    Document type Book
    Note Open-captioned. ; Title from title screen (viewed Apr. 9, 2009). ; Streaming video (1 hr., 39 sec. : sd., col.).
    Database Catalogue of the US National Library of Medicine (NLM)

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  9. Article ; Online: TGF-beta can leave you breathless.

    Qian, Bi-Feng / Wahl, Sharon M

    Current opinion in pharmacology

    2009  Volume 9, Issue 4, Page(s) 454–461

    Abstract: Transforming growth factor-beta (TGF-beta), a ubiquitous and multifunctional cytokine, is central to the evolution and modulation of host defense. Early on, TGF-beta was recognized for its chemotactic and pro-inflammatory properties, but then ... ...

    Abstract Transforming growth factor-beta (TGF-beta), a ubiquitous and multifunctional cytokine, is central to the evolution and modulation of host defense. Early on, TGF-beta was recognized for its chemotactic and pro-inflammatory properties, but then identification of its powerful suppressive activities focused attention on dissecting its mechanisms of immune inhibition. Just as quickly as TGF-beta-mediated regulation of a population of CD4(+)CD25(+)Foxp3(+) regulatory T cells became the rage, a surprising finding that TGF-beta was the impetus behind a subset of pro-inflammatory T helper (Th)17 cells brought back a re-emphasis on its broader ability to dictate inflammatory events. Emerging evidence indicates that much remains to be discovered regarding the complex and intertwined roles of TGF-beta in inflammation, T cell lineage commitment, antibody generation, immune suppression, and tolerance. While it may appear that TGF-beta has multiple, ill-defined, contradictory and overlapping modes of activity that are impossible to unravel, the current excitement for dissecting how TGF-beta controls immunity defines a challenge worthy of pursuit. The lung is particularly vulnerable to the influences of TGF-beta, which is produced by its immune and non-immune cell populations. In its absence, lung pathology becomes lethal, whereas TGF-beta overproduction also has untoward consequences, potentially leaving one breathless, and underscoring the paradoxical, but essential contribution of TGF-beta to tissue and immune homeostasis.
    MeSH term(s) Animals ; Antibody Formation/immunology ; Cell Differentiation/immunology ; Humans ; Immune Tolerance/immunology ; Inflammation Mediators/adverse effects ; Inflammation Mediators/physiology ; Respiration/immunology ; Respiration Disorders/immunology ; Respiration Disorders/metabolism ; Respiration Disorders/pathology ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; Transforming Growth Factor beta/physiology
    Chemical Substances Inflammation Mediators ; Transforming Growth Factor beta
    Language English
    Publishing date 2009-05-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2037057-X
    ISSN 1471-4973 ; 1471-4892
    ISSN (online) 1471-4973
    ISSN 1471-4892
    DOI 10.1016/j.coph.2009.04.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Transforming growth factor-beta-induced regulatory T cells referee inflammatory and autoimmune diseases.

    Wahl, Sharon M / Chen, Wanjun

    Arthritis research & therapy

    2005  Volume 7, Issue 2, Page(s) 62–68

    Abstract: Naturally occurring CD4+CD25+ regulatory T cells mediate immune suppression to limit immunopathogenesis associated with chronic inflammation, persistent infections and autoimmune diseases. Their mode of suppression is contact-dependent, antigen- ... ...

    Abstract Naturally occurring CD4+CD25+ regulatory T cells mediate immune suppression to limit immunopathogenesis associated with chronic inflammation, persistent infections and autoimmune diseases. Their mode of suppression is contact-dependent, antigen-nonspecific and involves a nonredundant contribution from the cytokine transforming growth factor (TGF)-beta. Not only can TGF-beta mediate cell-cell suppression between the regulatory T cells and CD4+CD25- or CD8+ T cells, but new evidence also reveals its role in the conversion of CD4+CD25- T cells, together with TCR antigen stimulation, into the regulatory phenotype. Elemental to this conversion process is induction of expression of the forkhead transcription factor, Foxp3. This context-dependent coercion of naive CD4+ T cells into a powerful subset of regulatory cells provides a window into potential manipulation of these cells to orchestrate therapeutic intervention in diseases characterized by inadequate suppression, as well as a promising means of controlling pathologic situations in which excessive suppression dominates.
    MeSH term(s) Animals ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/therapy ; Asthma/therapy ; Autoimmune Diseases/immunology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Clonal Anergy ; Disease Models, Animal ; Forkhead Transcription Factors/biosynthesis ; Forkhead Transcription Factors/genetics ; Gene Expression Regulation ; Humans ; Immune Tolerance/immunology ; Immunotherapy, Adoptive ; Inflammation/immunology ; Lupus Erythematosus, Systemic/immunology ; Mice ; Mice, Knockout ; Receptors, Interleukin-2/analysis ; Signal Transduction/physiology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/transplantation ; Transforming Growth Factor beta/physiology
    Chemical Substances FOXP3 protein, human ; Forkhead Transcription Factors ; Receptors, Interleukin-2 ; Transforming Growth Factor beta
    Language English
    Publishing date 2005-01-24
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2107602-9
    ISSN 1478-6362 ; 1478-6354
    ISSN (online) 1478-6362
    ISSN 1478-6354
    DOI 10.1186/ar1504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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