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  1. Article ; Online: Editorial overview: Autoimmunity.

    Haskins, Kathryn / Buckner, Jane Hoyt

    Current opinion in immunology

    2016  Volume 43, Page(s) v–vii

    MeSH term(s) Autoimmune Diseases ; Autoimmunity ; Humans
    Language English
    Publishing date 2016-11-10
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2016.10.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2773: Show issues Location:
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    Zs.MG 13: Show issues

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  2. Article ; Online: Mechanisms of impaired regulation by CD4(+)CD25(+)FOXP3(+) regulatory T cells in human autoimmune diseases.

    Buckner, Jane Hoyt

    Nature reviews. Immunology

    2010  Volume 10, Issue 12, Page(s) 849–859

    Abstract: A lack of regulatory T (T(Reg)) cells that express CD4, CD25 and forkhead box P3 (FOXP3) results in severe autoimmunity in both mice and humans. Since the discovery of T(Reg) cells, there has been intense investigation aimed at determining how they ... ...

    Abstract A lack of regulatory T (T(Reg)) cells that express CD4, CD25 and forkhead box P3 (FOXP3) results in severe autoimmunity in both mice and humans. Since the discovery of T(Reg) cells, there has been intense investigation aimed at determining how they protect an organism from autoimmunity and whether defects in their number or function contribute to the development of autoimmunity in model systems. The next phase of investigation - that is, to define the role that defects in T(Reg) cells have in human autoimmunity - is now underway. This Review summarizes our progress so far towards understanding the role of CD4(+)CD25(+)FOXP3(+) T(Reg) cells in human autoimmune diseases and the impact that this knowledge might have on the diagnosis and treatment of these diseases.
    MeSH term(s) Animals ; Autoimmune Diseases/diagnosis ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; CD4 Antigens/metabolism ; Forkhead Transcription Factors/metabolism ; Humans ; Inflammatory Bowel Diseases/immunology ; Interleukin-2 Receptor alpha Subunit/metabolism ; Mice ; Psoriasis/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances CD4 Antigens ; FOXP3 protein, human ; Forkhead Transcription Factors ; Interleukin-2 Receptor alpha Subunit
    Language English
    Publishing date 2010-12-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/nri2889
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 34: Show issues

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  3. Article: Lineage and signal strength determine the inhibitory effect of transforming growth factor beta1 (TGF-beta1) on human antigen-specific Th1 and Th2 memory cells.

    Holzer, Ursula / Rieck, Mary / Buckner, Jane Hoyt

    Journal of autoimmunity

    2006  Volume 26, Issue 4, Page(s) 241–251

    Abstract: TGF-beta1 is a pleotrophic cytokine playing an important role in immune regulation. The impact of TGF-beta1 on immune function is determined by the cell type and the microenvironment. CD4+ T cells exemplify this, by responding to TGF-beta1 in ... ...

    Abstract TGF-beta1 is a pleotrophic cytokine playing an important role in immune regulation. The impact of TGF-beta1 on immune function is determined by the cell type and the microenvironment. CD4+ T cells exemplify this, by responding to TGF-beta1 in heterogeneous ways based on their level of maturation and state of differentiation. TGF-beta1 leads to suppression of proliferation and cytokine production of naive T cells and influences the outcome of T cell differentiation. In mice, the response of memory T cells to TGF-beta1 is determined by the lineage of the cells. TGF-beta1 causes decreased proliferation of Th1 cells but has little effect on the proliferation of Th2 cells. Here we examined the effect of TGF-beta1 on human Th1 and Th2 memory T cells and show that proliferation of Th1 clones are inhibited by TGF-beta1, whereas Th2 cells are not. Furthermore the sensitivity of individual Th1 clones to TGF-beta1 is linked to the level of activation achieved in culture, but these differences cannot be explained by T cell receptor (TCR) affinity alone. Together this demonstrates that the human T cell response to TGF-beta1 is determined by the environment in which an immune response takes place and the previous immune experience of the cells involved.
    MeSH term(s) Animals ; Cell Cycle/drug effects ; Cell Cycle/immunology ; Cell Lineage ; Drosophila ; Epitopes, T-Lymphocyte/immunology ; Genes, MHC Class II/immunology ; Humans ; Immunologic Memory/immunology ; Interleukin-4/immunology ; Lymphocyte Activation/drug effects ; Receptors, Antigen, T-Cell/immunology ; Th1 Cells/cytology ; Th1 Cells/drug effects ; Th1 Cells/immunology ; Th2 Cells/cytology ; Th2 Cells/drug effects ; Th2 Cells/immunology ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/pharmacology ; Transforming Growth Factor beta1
    Chemical Substances Epitopes, T-Lymphocyte ; Receptors, Antigen, T-Cell ; TGFB1 protein, human ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Interleukin-4 (207137-56-2)
    Language English
    Publishing date 2006-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639452-8
    ISSN 0896-8411
    ISSN 0896-8411
    DOI 10.1016/j.jaut.2006.03.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2368: Show issues Location:
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  4. Article ; Online: In active relapsing-remitting multiple sclerosis, effector T cell resistance to adaptive T(regs) involves IL-6-mediated signaling.

    Schneider, Anya / Long, Sarah Alice / Cerosaletti, Karen / Ni, Chester T / Samuels, Peter / Kita, Mariko / Buckner, Jane Hoyt

    Science translational medicine

    2013  Volume 5, Issue 170, Page(s) 170ra15

    Abstract: Patients with multiple sclerosis (MS) manifest demyelination and neurodegeneration mediated in part by CD4(+) T cells that have escaped regulation. Resistance of pathogenic effector T cells (T(effs)) to suppression by regulatory T cells (T(regs)) has ... ...

    Abstract Patients with multiple sclerosis (MS) manifest demyelination and neurodegeneration mediated in part by CD4(+) T cells that have escaped regulation. Resistance of pathogenic effector T cells (T(effs)) to suppression by regulatory T cells (T(regs)) has been demonstrated in several autoimmune diseases. Although impairment in T(reg) number and function has been observed in relapsing-remitting MS (RRMS), T(eff) resistance has not been well studied in this disease. To determine whether T(eff) resistance contributes to failed tolerance in RRMS, we performed T(reg) suppression assays with T(effs) from either RRMS patients not on immunomodulatory therapy or healthy individuals. T(eff) resistance was present in the T(effs) of RRMS patients with active disease but not from patients with inactive disease. Interleukin-6 (IL-6) and phosphorylation of signal transducer and activator of transcription 3 (pSTAT3) promote T(eff) resistance to T(regs), and we found an increase in IL-6 receptor α (IL-6Rα) expression and elevated IL-6 signaling as measured by pSTAT3 in our RRMS subjects. Further, the impaired suppression in RRMS subjects correlated with an increase in IL-6Rα surface expression on CD4(+) T cells and an increase in pSTAT3 in response to IL-6. To address whether the enhanced pSTAT3 contributed to T(eff) resistance in active RRMS patients, we blocked STAT3 phosphorylation and found that impaired suppression was reversed. Therefore, enhanced IL-6R signaling through pSTAT3, in some cases through increased IL-6Rα expression, contributed to T(eff) resistance in active RRMS. These markers may aid in determining disease activity and responsiveness to immunomodulatory therapies in RRMS.
    MeSH term(s) Forkhead Transcription Factors/metabolism ; Humans ; Interleukin-6/metabolism ; Multiple Sclerosis, Relapsing-Remitting/immunology ; Multiple Sclerosis, Relapsing-Remitting/pathology ; Phosphorylation ; Receptors, Interleukin-6/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances FOXP3 protein, human ; Forkhead Transcription Factors ; Interleukin-6 ; Receptors, Interleukin-6 ; STAT3 Transcription Factor ; interleukin-6 receptor alpha
    Language English
    Publishing date 2013-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.3004970
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6941: Show issues Location:
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  5. Article ; Online: Mice expressing HLA-DQ6alpha8beta transgenes develop polychondritis spontaneously.

    Lamoureux, Jennifer L / Buckner, Jane Hoyt / David, Chella S / Bradley, David S

    Arthritis research & therapy

    2006  Volume 8, Issue 4, Page(s) R134

    Abstract: Relapsing polychondritis (RP) is a human autoimmune disease of unknown etiology in which cartilaginous sites are destroyed by cyclic inflammatory episodes beginning, most commonly, during the fourth or fifth decade of life. We have previously described ... ...

    Abstract Relapsing polychondritis (RP) is a human autoimmune disease of unknown etiology in which cartilaginous sites are destroyed by cyclic inflammatory episodes beginning, most commonly, during the fourth or fifth decade of life. We have previously described collagen-induced polychondritis that closely mirrors RP occurring in young (6-8 weeks old) HLA-DQ6alphabeta 8alphabeta transgenic Abeta0 mice, following immunization with heterologous type II collagen (CII). We present evidence here that transgenic strains expressing the DQ6alpha8beta transgene develop spontaneous polychondritis (SP) at the mouse equivalent of human middle age (4.5-6 months and 40-50 years old, respectively) and display polyarthritis, auricular chondritis and nasal chondritis--three of the most common sites affected in RP. Auricular chondritis in SP, like RP but unlike CII-induced polychondritis, exhibited a relapsing/remitting phenotype, requiring several inflammatory cycles before the cartilage is destroyed. Elevated serum levels of total IgG corresponded with the onset of disease in SP, as in RP and CII-induced polychondritis. No CII-specific immune response was detected in SP, however--more closely mirroring RP, in which as few as 30% of RP patients have been reported to have CII-specific IgG. CII-induced polychondritis displays a strong CII-specific immune response. SP also demonstrated a strong female preponderance, as some workers have reported in RP but has not observed in CII-induced polychondritis. These characteristics of SP allow for the examination of the immunopathogenesis of polychondritis in the absence of an overwhelming CII-specific immune response and the strong adjuvant-induced immunostimulatory influence in CII-induced polychondritis. This spontaneous model of polychondritis provides a new and unique tool to investigate both the initiatory events as well as the immunopathogenic mechanisms occurring at cartilaginous sites during the cyclic inflammatory assaults of polychondritis.
    MeSH term(s) Animals ; Cartilage/pathology ; Disease Models, Animal ; Ear Cartilage/pathology ; Female ; HLA-DQ Antigens/genetics ; Immunoglobulin G/blood ; Male ; Mice ; Mice, Transgenic/genetics ; Nose ; Phenotype ; Polychondritis, Relapsing/blood ; Polychondritis, Relapsing/genetics ; Polychondritis, Relapsing/pathology ; Sex Factors ; Transgenes
    Chemical Substances HLA-DQ Antigens ; HLA-DQ6 antigen ; Immunoglobulin G
    Language English
    Publishing date 2006
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2107602-9
    ISSN 1478-6362 ; 1478-6354
    ISSN (online) 1478-6362
    ISSN 1478-6354
    DOI 10.1186/ar2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5490: Show issues Location:
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  6. Article: Differential antigen sensitivity and costimulatory requirements in human Th1 and Th2 antigen-specific CD4+ cells with similar TCR avidity.

    Holzer, Ursula / Kwok, William W / Nepom, Gerald T / Buckner, Jane Hoyt

    Journal of immunology (Baltimore, Md. : 1950)

    2003  Volume 170, Issue 3, Page(s) 1218–1223

    Abstract: The differentiation of naive CD4(+) Th cells into Th1 and Th2 phenotypes is influenced by cytokines, concentration of Ag, accessory molecules, and the affinity of the MHC-TCR interaction. To study these factors in human memory T cells, T cell lines with ... ...

    Abstract The differentiation of naive CD4(+) Th cells into Th1 and Th2 phenotypes is influenced by cytokines, concentration of Ag, accessory molecules, and the affinity of the MHC-TCR interaction. To study these factors in human memory T cells, T cell lines with Th1 or Th2 phenotypes specific for the peptide hemagglutinin (HA)(307-319) in the context of DRB1*0401 were established from the peripheral blood of an individual previously vaccinated for influenza virus. Flow cytometric analysis with fluorescent-labeled MHC class II tetramers was used to analyze TCR avidity: the Th2 line bound the HLA-DR*0401-HA(307-319) tetramers with higher mean avidity, although the range of binding avidity largely overlapped with the Th1 line. High-affinity Th1 and Th2 lines were established for further study by FACS sorting. When activated with plate-bound HLA-DR*0401-HA(307-319) monomers, the Th1 line proliferated and produced IFN-gamma without additional costimulation whereas the Th2 line required the addition of soluble anti-CD28 Ab to induce proliferation and IL-5 production, but this requirement could be overcome with high concentrations of plate-bound monomer alone. IL-2 production was dependent on costimulation in both cell lines. These findings demonstrate that upon antigenic rechallenge, Th1 and Th2 cells differ in their response to Ag-specific stimulation. Th2 cells were sensitive to the strength of signal to a greater degree than Th1 cells and required costimulation through CD28 for maximal proliferation. These distinctions between Th1 and Th2 activation are not consistent with a simple avidity model of Ag recognition and indicate both qualitative and quantitative differences in determining cell lineage commitment.
    MeSH term(s) Cell Differentiation/immunology ; Cell Division/immunology ; Cell Lineage/immunology ; Cells, Cultured ; Epitopes, T-Lymphocyte/immunology ; Hemagglutinin Glycoproteins, Influenza Virus ; Hemagglutinins, Viral/immunology ; Hemagglutinins, Viral/pharmacology ; Humans ; Immunologic Memory ; Lymphocyte Activation/immunology ; Peptide Fragments/immunology ; Peptide Fragments/pharmacology ; Protein Binding/immunology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Th1 Cells/immunology ; Th1 Cells/metabolism ; Th1 Cells/virology ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Th2 Cells/virology
    Chemical Substances Epitopes, T-Lymphocyte ; Hemagglutinin Glycoproteins, Influenza Virus ; Hemagglutinins, Viral ; Peptide Fragments ; Receptors, Antigen, T-Cell, alpha-beta ; influenza hemagglutinin (307-319)
    Language English
    Publishing date 2003-01-14
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    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.170.3.1218
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 28: Show issues

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