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  1. AU="Greaves, Sarah A"
  2. AU="Cai, Simin"
  3. AU="Casner, Nancy"
  4. AU="Jiawen Cheng"
  5. AU="Portela, Gerard T"
  6. AU="Huang, W. H."
  7. AU=Chen Ji-Wang AU=Chen Ji-Wang
  8. AU="Naeem Aziz Memon"
  9. AU="Ficorella, F."
  10. AU="McArthur, Brae Anne"
  11. AU="Otero-González, J"
  12. AU="Klco, Peter"
  13. AU="Tirado-Amador, Lesbia"
  14. AU="Dambrin, Camille"
  15. AU="Shaw, Liz"
  16. AU="Wand, Taylor"
  17. AU="Zou, Fengqian"
  18. AU="Brisson, Julien B"
  19. AU="Khoshakhlagh, Parastoo"
  20. AU="Shah, Sejal S"
  21. AU="Marshall, Leigh"
  22. AU="Zamorano Soto, Pedro"
  23. AU="Deng, Wenwei"
  24. AU="Means, Robert E"
  25. AU="Aaltonen, Tarja"
  26. AU="March, Sonja"
  27. AU="Pieper, Carl"
  28. AU="Marsicano, Giovanni"
  29. AU="Karagöl, Alper"
  30. AU="Cutlip, Donald E"
  31. AU="Sayan Chatterjee"
  32. AU="Köstler, Josef"
  33. AU="Conboy, Erin"
  34. AU=Martinot Martin
  35. AU="Heller, R."
  36. AU="Mo, Jinping"
  37. AU="Lui, Wen"
  38. AU="Strati, V."
  39. AU="Dixon, Matthew W.A"
  40. AU=da Mata Kanzaki Elida C G
  41. AU="ElenaTourkina"
  42. AU="Chu, Yaojuan"
  43. AU="Bakker, Michiel A."
  44. AU=Hill W Cary AU=Hill W Cary
  45. AU="Hand, Marissa"
  46. AU="Guerra, Giselle"
  47. AU="Allouch, Asma"

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  1. Artikel ; Online: Adaptive Immunity in Pulmonary Sarcoidosis and Chronic Beryllium Disease.

    Greaves, Sarah A / Atif, Shaikh M / Fontenot, Andrew P

    Frontiers in immunology

    2020  Band 11, Seite(n) 474

    Abstract: Pulmonary sarcoidosis and chronic beryllium disease (CBD) are inflammatory granulomatous lung diseases defined by the presence of non-caseating granulomas in the lung. CBD results from beryllium exposure in the workplace, while the cause of sarcoidosis ... ...

    Abstract Pulmonary sarcoidosis and chronic beryllium disease (CBD) are inflammatory granulomatous lung diseases defined by the presence of non-caseating granulomas in the lung. CBD results from beryllium exposure in the workplace, while the cause of sarcoidosis remains unknown. CBD and sarcoidosis are both immune-mediated diseases that involve Th1-polarized inflammation in the lung. Beryllium exposure induces trafficking of dendritic cells to the lung in a mechanism dependent on MyD88 and IL-1α. B cells are also recruited to the lung in a MyD88 dependent manner after beryllium exposure in order to protect the lung from beryllium-induced injury. Similar to most immune-mediated diseases, disease susceptibility in CBD and sarcoidosis is driven by the expression of certain MHCII molecules, primarily
    Mesh-Begriff(e) Adaptive Immunity ; Animals ; Berylliosis/immunology ; Chronic Disease ; HLA-DP beta-Chains/genetics ; Humans ; Lung/immunology ; Sarcoidosis, Pulmonary/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/immunology
    Chemische Substanzen HLA-DP beta-Chains ; HLA-DPB1 antigen
    Sprache Englisch
    Erscheinungsdatum 2020-03-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.00474
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: B-cell intrinsic and extrinsic signals that regulate central tolerance of mouse and human B cells.

    Pelanda, Roberta / Greaves, Sarah A / Alves da Costa, Thiago / Cedrone, Lena M / Campbell, Margaret L / Torres, Raul M

    Immunological reviews

    2022  Band 307, Heft 1, Seite(n) 12–26

    Abstract: The random recombination of immunoglobulin V(D)J gene segments produces unique IgM antibodies that serve as the antigen receptor for each developing B cell. Hence, the newly formed B cell repertoire is comprised of a variety of specificities that display ...

    Abstract The random recombination of immunoglobulin V(D)J gene segments produces unique IgM antibodies that serve as the antigen receptor for each developing B cell. Hence, the newly formed B cell repertoire is comprised of a variety of specificities that display a range of reactivity with self-antigens. Newly generated IgM
    Mesh-Begriff(e) Autoimmunity ; B-Lymphocytes ; Bone Marrow Cells ; Central Tolerance ; Humans ; Precursor Cells, B-Lymphoid/metabolism ; Receptors, Antigen, B-Cell/metabolism
    Chemische Substanzen Receptors, Antigen, B-Cell
    Sprache Englisch
    Erscheinungsdatum 2022-01-08
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/imr.13062
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Activation of the MEK-ERK Pathway Is Necessary but Not Sufficient for Breaking Central B Cell Tolerance.

    Greaves, Sarah A / Peterson, Jacob N / Torres, Raul M / Pelanda, Roberta

    Frontiers in immunology

    2018  Band 9, Seite(n) 707

    Abstract: Newly generated bone marrow B cells are positively selected into the peripheral lymphoid tissue only when they express a B cell receptor (BCR) that is nonautoreactive or one that binds self-antigen with only minimal avidity. This positive selection ... ...

    Abstract Newly generated bone marrow B cells are positively selected into the peripheral lymphoid tissue only when they express a B cell receptor (BCR) that is nonautoreactive or one that binds self-antigen with only minimal avidity. This positive selection process, moreover, is critically contingent on the ligand-independent tonic signals transduced by the BCR. We have previously shown that when autoreactive B cells express an active form of the rat sarcoma (RAS) oncogene, they upregulate the receptor for the B cell activating factor (BAFFR) and undergo differentiation
    Mesh-Begriff(e) Animals ; Antibody Formation ; B-Cell Activation Factor Receptor/genetics ; B-Cell Activation Factor Receptor/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Central Tolerance/immunology ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Gene Expression Regulation ; Genetic Vectors/genetics ; MAP Kinase Signaling System ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Receptors, Antigen, B-Cell/genetics ; Receptors, Antigen, B-Cell/metabolism ; Retroviridae/genetics ; Signal Transduction ; Transduction, Genetic ; Transgenes
    Chemische Substanzen B-Cell Activation Factor Receptor ; Receptors, Antigen, B-Cell ; Tnfrsf13c protein, mouse ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Sprache Englisch
    Erscheinungsdatum 2018-04-09
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.00707
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Corrigendum: Activation of the MEK-ERK Pathway Is Necessary but Not Sufficient for Breaking Central B Cell Tolerance.

    Greaves, Sarah A / Peterson, Jacob N / Torres, Raul M / Pelanda, Roberta

    Frontiers in immunology

    2018  Band 9, Seite(n) 2218

    Abstract: This corrects the article DOI: 10.3389/fimmu.2018.00707.]. ...

    Abstract [This corrects the article DOI: 10.3389/fimmu.2018.00707.].
    Sprache Englisch
    Erscheinungsdatum 2018-09-27
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Published Erratum
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.02218
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Active PI3K abrogates central tolerance in high-avidity autoreactive B cells.

    Greaves, Sarah A / Peterson, Jacob N / Strauch, Pamela / Torres, Raul M / Pelanda, Roberta

    The Journal of experimental medicine

    2019  Band 216, Heft 5, Seite(n) 1135–1153

    Abstract: Autoreactive B cells that bind self-antigen with high avidity in the bone marrow undergo mechanisms of central tolerance that prevent their entry into the peripheral B cell population. These mechanisms are breached in many autoimmune patients, increasing ...

    Abstract Autoreactive B cells that bind self-antigen with high avidity in the bone marrow undergo mechanisms of central tolerance that prevent their entry into the peripheral B cell population. These mechanisms are breached in many autoimmune patients, increasing their risk of B cell-mediated autoimmune diseases. Resolving the molecular pathways that can break central B cell tolerance could therefore provide avenues to diminish autoimmunity. Here, we show that B cell-intrinsic expression of a constitutively active form of PI3K-P110α by high-avidity autoreactive B cells of mice completely abrogates central B cell tolerance and further promotes these cells to escape from the bone marrow, differentiate in peripheral tissue, and undergo activation in response to self-antigen. Upon stimulation with T cell help factors, these B cells secrete antibodies in vitro but remain unable to secrete autoantibodies in vivo. Overall, our data demonstrate that activation of the PI3K pathway leads high-avidity autoreactive B cells to breach central, but not late, stages of peripheral tolerance.
    Mesh-Begriff(e) Animals ; Autoantibodies/immunology ; Autoantigens/immunology ; Autoimmunity/immunology ; B-Lymphocytes/immunology ; Bone Marrow Cells/metabolism ; Cell Differentiation/immunology ; Central Tolerance/immunology ; Class Ia Phosphatidylinositol 3-Kinase/metabolism ; Female ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Animal ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Complement 3d/metabolism ; Spleen/cytology ; T-Lymphocytes/immunology
    Chemische Substanzen Autoantibodies ; Autoantigens ; Receptors, Antigen, B-Cell ; Receptors, Complement 3d ; Class Ia Phosphatidylinositol 3-Kinase (EC 2.7.1.137)
    Sprache Englisch
    Erscheinungsdatum 2019-04-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20181652
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: CD4+ T cells in the lungs of acute sarcoidosis patients recognize an Aspergillus nidulans epitope.

    Greaves, Sarah A / Ravindran, Avinash / Santos, Radleigh G / Chen, Lan / Falta, Michael T / Wang, Yang / Mitchell, Angela M / Atif, Shaikh M / Mack, Douglas G / Tinega, Alex N / Maier, Lisa A / Dai, Shaodong / Pinilla, Clemencia / Grunewald, Johan / Fontenot, Andrew P

    The Journal of experimental medicine

    2021  Band 218, Heft 10

    Abstract: Löfgren's syndrome (LS) is an acute form of sarcoidosis characterized by a genetic association with HLA-DRB1*03 (HLA-DR3) and an accumulation of CD4+ T cells of unknown specificity in the bronchoalveolar lavage (BAL). Here, we screened related LS- ... ...

    Abstract Löfgren's syndrome (LS) is an acute form of sarcoidosis characterized by a genetic association with HLA-DRB1*03 (HLA-DR3) and an accumulation of CD4+ T cells of unknown specificity in the bronchoalveolar lavage (BAL). Here, we screened related LS-specific TCRs for antigen specificity and identified a peptide derived from NAD-dependent histone deacetylase hst4 (NDPD) of Aspergillus nidulans that stimulated these CD4+ T cells in an HLA-DR3-restricted manner. Using ELISPOT analysis, a greater number of IFN-γ- and IL-2-secreting T cells in the BAL of DR3+ LS subjects compared with DR3+ control subjects was observed in response to the NDPD peptide. Finally, increased IgG antibody responses to A. nidulans NDPD were detected in the serum of DR3+ LS subjects. Thus, our findings identify a ligand for CD4+ T cells derived from the lungs of LS patients and suggest a role of A. nidulans in the etiology of LS.
    Mesh-Begriff(e) Adult ; Animals ; Antigens, Fungal/immunology ; Aspergillus nidulans/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/microbiology ; Case-Control Studies ; Epitopes, T-Lymphocyte/immunology ; Female ; Fungal Proteins/immunology ; HLA-DR3 Antigen/chemistry ; HLA-DR3 Antigen/genetics ; HLA-DR3 Antigen/immunology ; Humans ; Hybridomas/immunology ; Immunoglobulin G ; Male ; Mice, Transgenic ; Middle Aged ; Sarcoidosis/immunology
    Chemische Substanzen Antigens, Fungal ; Epitopes, T-Lymphocyte ; Fungal Proteins ; HLA-DR3 Antigen ; Immunoglobulin G
    Sprache Englisch
    Erscheinungsdatum 2021-08-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20210785
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Activation of Ras overcomes B-cell tolerance to promote differentiation of autoreactive B cells and production of autoantibodies.

    Teodorovic, Lenka S / Babolin, Chiara / Rowland, Sarah L / Greaves, Sarah A / Baldwin, David P / Torres, Raul M / Pelanda, Roberta

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

    2014  Band 111, Heft 27, Seite(n) E2797–806

    Abstract: Newly generated immature B cells are selected to enter the peripheral mature B-cell pool only if they do not bind (or bind limited amount of) self-antigen. We previously suggested that this selection relies on basal extracellular signal-regulated kinase ( ...

    Abstract Newly generated immature B cells are selected to enter the peripheral mature B-cell pool only if they do not bind (or bind limited amount of) self-antigen. We previously suggested that this selection relies on basal extracellular signal-regulated kinase (Erk) activation mediated by tonic B-cell antigen receptor (BCR) signaling and that this signal can be replaced by an active rat sarcoma (Ras), which are small GTPase proteins. In this study we compared the activity of Ras and Erk in nonautoreactive and autoreactive immature B cells and investigated whether activation of Ras can break tolerance. Our results demonstrate lower levels of active Erk and Ras in autoreactive immature B cells, although this is evident only when these cells display medium/high avidity for self-antigen. Basal activation of Erk in immature B cells is proportional to surface IgM and dependent on sarcoma family kinases, whereas it is independent of B-cell activating factor, IFN, and Toll-like receptor signaling. Ectopic expression of the constitutively active mutant Ras form N-RasD12 in autoreactive cells raises active Erk, halts receptor editing via PI3 kinase, and promotes differentiation via Erk, breaking central tolerance. Moreover, when B cells coexpress autoreactive and nonautoreactive BCRs, N-RasD12 leads also to a break in peripheral tolerance with the production of autoantibodies. Our findings indicate that in immature B cells, basal activation of Ras and Erk are controlled by tonic BCR signaling, and that positive changes in Ras activity can lead to a break in both central and peripheral B-cell tolerance.
    Mesh-Begriff(e) Animals ; Autoantibodies/biosynthesis ; B-Lymphocytes/immunology ; Bone Marrow Cells/metabolism ; Cell Differentiation ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Immune Tolerance ; Phosphatidylinositol 3-Kinases/metabolism ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Signal Transduction ; ras Proteins/metabolism
    Chemische Substanzen Autoantibodies ; Receptors, Antigen, B-Cell ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; ras Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2014-06-23
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1402159111
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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