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  1. Article ; Online: Innate B cells cleave to the marginal zone.

    DeFranco, Anthony L

    Nature immunology

    2017  Volume 18, Issue 3, Page(s) 248–250

    Language English
    Publishing date 2017-02-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/ni.3685
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  2. Article: Multilayer Control of B Cell Activation by the B Cell Antigen Receptor: Following Themes Initiated With Bill Paul.

    DeFranco, Anthony L

    Frontiers in immunology

    2018  Volume 9, Page(s) 739

    Abstract: This article describes the work I did in Bill Paul's lab as a postdoctoral fellow between 1979 and 1983, and to a lesser extent puts that work in the context of other work on B cell activation and antibody responses that was going on in Bill's lab at ... ...

    Abstract This article describes the work I did in Bill Paul's lab as a postdoctoral fellow between 1979 and 1983, and to a lesser extent puts that work in the context of other work on B cell activation and antibody responses that was going on in Bill's lab at that time and shortly beforehand, including the discovery of interleukin 4. In addition, this work describes the subsequent and continuing work in my own lab following-up on themes I began during my time working directly with Bill. A particular emphasis was on understanding the biochemical mechanisms of signaling by the B cell antigen receptor (BCR) to the interior of the B cell. Some of the studies from my lab related to the regulation of BCR signaling by Lyn are described in relationship to the lymphocyte tuning hypothesis put forth by Grossman and Paul in 1992 and subsequently.
    MeSH term(s) Allergy and Immunology/history ; B-Lymphocytes/immunology ; History, 20th Century ; History, 21st Century ; Lymphocyte Activation ; Receptors, Antigen, B-Cell/immunology
    Chemical Substances Receptors, Antigen, B-Cell
    Language English
    Publishing date 2018-04-23
    Publishing country Switzerland
    Document type Biography ; Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.00739
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: Immunity

    DeFranco, Anthony L. / Locksley, Richard M. / Robertson, Miranda

    the immune response in infectious and inflammatory disease

    (Primers in biology)

    2007  

    Author's details Anthony L. DeFranco ; Richard M. Locksley ; Miranda Robertson
    Series title Primers in biology
    Keywords Immune system ; Immunreaktion
    Subject Abwehrreaktion ; Immunantwort ; Immunoreaktivität ; Immunabwehr
    Subject code 571.9646
    Language English
    Size XXX, 387 S., [1] Bl. : zahlr. Ill., 28cm
    Publisher New Science Press u.a.
    Publishing place London
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT014855759
    ISBN 0-19-920614-7 ; 978-0-19-920614-8 ; 0-9539181-0-6 ; 978-0-9539181-0-2 ; 0-87893-179-1 ; 978-0-87893-179-8
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2007 A 2099 order for loan Magazin

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  4. Article ; Online: Tracking the role of Aire in immune tolerance to the eye with a TCR transgenic mouse model.

    Yin, Mianmian / Smith, Jennifer A / Chou, Marissa / Chan, Jackie / Jittayasothorn, Yingyos / Gould, Douglas B / Caspi, Rachel R / Anderson, Mark S / DeFranco, Anthony L

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Volume 121, Issue 5, Page(s) e2311487121

    Abstract: Roughly one-half of mice with partial defects in two immune tolerance pathways ( ... ...

    Abstract Roughly one-half of mice with partial defects in two immune tolerance pathways (Aire
    MeSH term(s) Animals ; Mice ; Antigen Presentation ; Autoantigens ; Disease Models, Animal ; Mice, Inbred Strains ; Mice, Transgenic ; Receptors, Antigen, T-Cell
    Chemical Substances Autoantigens ; Receptors, Antigen, T-Cell ; Aire protein, mouse
    Language English
    Publishing date 2024-01-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2311487121
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  5. Article: The germinal center antibody response in health and disease.

    DeFranco, Anthony L

    F1000Research

    2016  Volume 5

    Abstract: The germinal center response is the delayed but sustained phase of the antibody response that is responsible for producing high-affinity antibodies of the IgG, IgA and/or IgE isotypes. B cells in the germinal center undergo re-iterative cycles of somatic ...

    Abstract The germinal center response is the delayed but sustained phase of the antibody response that is responsible for producing high-affinity antibodies of the IgG, IgA and/or IgE isotypes. B cells in the germinal center undergo re-iterative cycles of somatic hypermutation of immunoglobulin gene variable regions, clonal expansion, and Darwinian selection for cells expressing higher-affinity antibody variants. Alternatively, selected B cells can terminally differentiate into long-lived plasma cells or into a broad diversity of mutated memory B cells; the former secrete the improved antibodies to fight an infection and to provide continuing protection from re-infection, whereas the latter may jumpstart immune responses to subsequent infections with related but distinct infecting agents. Our understanding of the molecules involved in the germinal center reaction has been informed by studies of human immunodeficiency patients with selective defects in the production of antibodies. Recent studies have begun to reveal how innate immune recognition via Toll-like receptors can enhance the magnitude and selective properties of the germinal center, leading to more effective control of infection by a subset of viruses. Just as early insights into the nature of the germinal center found application in the development of the highly successful conjugate vaccines, more recent insights may find application in the current efforts to develop new generations of vaccines, including vaccines that can induce broadly protective neutralizing antibodies against influenza virus or HIV-1.
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.7717.1
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  6. Article ; Online: Germinal centers and autoimmune disease in humans and mice.

    DeFranco, Anthony L

    Immunology and cell biology

    2016  Volume 94, Issue 10, Page(s) 918–924

    Abstract: Antibodies are involved in the pathogenesis of many autoimmune diseases. Although the mechanisms underlying the antibody response to infection or vaccination are reasonably well understood, we still have a poor understanding of the nature of autoimmune ... ...

    Abstract Antibodies are involved in the pathogenesis of many autoimmune diseases. Although the mechanisms underlying the antibody response to infection or vaccination are reasonably well understood, we still have a poor understanding of the nature of autoimmune antibody responses. The most well studied are the anti-nuclear antibody responses characteristic of systemic lupus erythematosus and studies over the past decade or so have demonstrated a critical role for signaling by TLR7 and/or TLR9 in B cells to promote these responses. These Toll-like receptors (TLRs) can promote T-cell-independent extrafollicular antibody responses with a heavy-chain class switch and a low degree of somatic mutation, but they can also strongly boost the germinal center response that gives rise to high-affinity antibodies and long-lived plasma cells. TLRs have been shown to enhance affinity maturation in germinal center responses to produce high-affinity neutralizing antibodies in several virus infection models of mice. Although more data are needed, it appears that anti-nuclear antibodies in mouse models of lupus and in lupus patients can be generated by either pathway, provided there are genetic susceptibility alleles that compromise B-cell tolerance at one or another stage. Limited data in other autoimmune diseases suggest that the germinal center response may be the predominant pathway leading to autoantibodies in those diseases. A better understanding of the mechanisms of autoantibody production may ultimately be helpful in the development of targeted therapeutics for lupus or other autoimmune diseases.
    MeSH term(s) Animals ; Antibody Formation/immunology ; Autoantibodies/biosynthesis ; Autoimmune Diseases/immunology ; B-Lymphocytes/immunology ; Germinal Center/immunology ; Humans ; Mice ; Toll-Like Receptors/metabolism
    Chemical Substances Autoantibodies ; Toll-Like Receptors
    Language English
    Publishing date 2016-08-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 284057-1
    ISSN 1440-1711 ; 0818-9641
    ISSN (online) 1440-1711
    ISSN 0818-9641
    DOI 10.1038/icb.2016.78
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  7. Article ; Online: Antigen Complexed with a TLR9 Agonist Bolsters c-Myc and mTORC1 Activity in Germinal Center B Lymphocytes.

    Wigton, Eric J / DeFranco, Anthony L / Ansel, K Mark

    ImmunoHorizons

    2019  Volume 3, Issue 8, Page(s) 389–401

    Abstract: The germinal center (GC) is the anatomical site where humoral immunity evolves. B cells undergo cycles of proliferation and selection to produce high-affinity Abs against Ag. Direct linkage of a TLR9 agonist (CpG) to a T-dependent Ag increases the number ...

    Abstract The germinal center (GC) is the anatomical site where humoral immunity evolves. B cells undergo cycles of proliferation and selection to produce high-affinity Abs against Ag. Direct linkage of a TLR9 agonist (CpG) to a T-dependent Ag increases the number of GC B cells. We used a T-dependent Ag complexed with CpG and a genetic model for ablating the TLR9 signaling adaptor molecule MyD88 specifically in B cells (B-MyD88
    MeSH term(s) Animals ; Antigens/chemistry ; Antigens/metabolism ; B-Lymphocytes/immunology ; Germinal Center/metabolism ; Ligands ; Lymphocyte Activation/immunology ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Signal Transduction/immunology ; T-Lymphocytes/immunology ; Toll-Like Receptor 9/agonists ; Transcriptome ; gamma-Globulins/immunology
    Chemical Substances Antigens ; Ligands ; Myc protein, mouse ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; Proto-Oncogene Proteins c-myc ; Tlr9 protein, mouse ; Toll-Like Receptor 9 ; gamma-Globulins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2019-08-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2573-7732
    ISSN (online) 2573-7732
    DOI 10.4049/immunohorizons.1900030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The germinal center antibody response in health and disease [version 1; referees

    Anthony L. DeFranco

    F1000Research, Vol

    2 approved]

    2016  Volume 5

    Abstract: The germinal center response is the delayed but sustained phase of the antibody response that is responsible for producing high-affinity antibodies of the IgG, IgA and/or IgE isotypes. B cells in the germinal center undergo re-iterative cycles of somatic ...

    Abstract The germinal center response is the delayed but sustained phase of the antibody response that is responsible for producing high-affinity antibodies of the IgG, IgA and/or IgE isotypes. B cells in the germinal center undergo re-iterative cycles of somatic hypermutation of immunoglobulin gene variable regions, clonal expansion, and Darwinian selection for cells expressing higher-affinity antibody variants. Alternatively, selected B cells can terminally differentiate into long-lived plasma cells or into a broad diversity of mutated memory B cells; the former secrete the improved antibodies to fight an infection and to provide continuing protection from re-infection, whereas the latter may jumpstart immune responses to subsequent infections with related but distinct infecting agents. Our understanding of the molecules involved in the germinal center reaction has been informed by studies of human immunodeficiency patients with selective defects in the production of antibodies. Recent studies have begun to reveal how innate immune recognition via Toll-like receptors can enhance the magnitude and selective properties of the germinal center, leading to more effective control of infection by a subset of viruses. Just as early insights into the nature of the germinal center found application in the development of the highly successful conjugate vaccines, more recent insights may find application in the current efforts to develop new generations of vaccines, including vaccines that can induce broadly protective neutralizing antibodies against influenza virus or HIV-1.
    Keywords Antigen Processing & Recognition ; Autoimmunity ; Drug Discovery & Design ; Genetics of the Immune System ; Immune Response ; Immunity to Infections ; Immunomodulation ; Immunopharmacology & Hematologic Pharmacology ; Leukocyte Activation ; Leukocyte Signaling & Gene Expression ; Medical Microbiology ; Protein Chemistry & Proteomics ; Virology ; Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2016-05-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Prolonged production of reactive oxygen species in response to B cell receptor stimulation promotes B cell activation and proliferation.

    Wheeler, Matthew L / Defranco, Anthony L

    Journal of immunology (Baltimore, Md. : 1950)

    2012  Volume 189, Issue 9, Page(s) 4405–4416

    Abstract: We have investigated the intracellular sources and physiological function of reactive oxygen species (ROS) produced in primary B cells in response to BCR stimulation. BCR stimulation of primary resting murine B cells induced the rapid production of ROS ... ...

    Abstract We have investigated the intracellular sources and physiological function of reactive oxygen species (ROS) produced in primary B cells in response to BCR stimulation. BCR stimulation of primary resting murine B cells induced the rapid production of ROS that occurred within minutes and was maintained for at least 24 h after receptor stimulation. While the early production of ROS (0-2 h) was dependent on the Nox2 isoform of NADPH oxidase, at later stages of B cell activation (6-24 h) ROS were generated by a second pathway, which appeared to be dependent on mitochondrial respiration. B cells from mice deficient in the Nox2 NADPH oxidase complex lacked detectable early production of extracellular and intracellular ROS after BCR stimulation but had normal proximal BCR signaling and BCR-induced activation and proliferation in vitro and mounted normal or somewhat elevated Ab responses in vivo. In contrast, neutralizing both pathways of BCR-derived ROS with the scavenger N-acetylcysteine resulted in impaired in vitro BCR-induced activation and proliferation and attenuated BCR signaling through the PI3K pathway at later times. These results indicate that the production of ROS downstream of the BCR is derived from at least two distinct cellular sources and plays a critical role at the later stages of B cell activation by promoting sustained BCR signaling via the PI3K pathway, which is needed for effective B cell responses to Ag.
    MeSH term(s) Animals ; B-Lymphocyte Subsets/cytology ; B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/metabolism ; Cell Proliferation ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mice, Transgenic ; Reactive Oxygen Species/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, B-Cell/physiology ; Signal Transduction/immunology ; Time Factors
    Chemical Substances Reactive Oxygen Species ; Receptors, Antigen, B-Cell
    Language English
    Publishing date 2012-09-28
    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.1201433
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    Ud II Zs.37: Show issues Location:
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  10. Article ; Online: "Dangerous crystals".

    DeFranco, Anthony L

    Immunity

    2008  Volume 29, Issue 5, Page(s) 670–671

    Abstract: Uric acid (UA) crystals are a potent stimulator of inflammation, but how they activate immune cells is not known. In this issue of Immunity, Ng et al. (2008) provide evidence suggesting that UA activates the Syk kinase via membrane cholesterol. ...

    Abstract Uric acid (UA) crystals are a potent stimulator of inflammation, but how they activate immune cells is not known. In this issue of Immunity, Ng et al. (2008) provide evidence suggesting that UA activates the Syk kinase via membrane cholesterol.
    MeSH term(s) Animals ; Cell Membrane/chemistry ; Cell Membrane/metabolism ; Cholesterol/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Fibroblasts/immunology ; Fibroblasts/metabolism ; Inflammation/immunology ; Intracellular Signaling Peptides and Proteins/metabolism ; Microscopy, Atomic Force ; Protein-Tyrosine Kinases/metabolism ; Syk Kinase ; Uric Acid/immunology ; Uric Acid/metabolism
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Uric Acid (268B43MJ25) ; Cholesterol (97C5T2UQ7J) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Syk Kinase (EC 2.7.10.2)
    Language English
    Publishing date 2008-11-14
    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.2008.10.005
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