Silvia Bolland

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc An innate path to human B cell tolerance
    Silvia Bolland
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Immunity 29:667-9. 2008
  2. pmc Vicious circle: systemic autoreactivity in Ro52/TRIM21-deficient mice
    Silvia Bolland
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville MD 20852, USA
    J Exp Med 206:1647-51. 2009
  3. pmc Control of toll-like receptor 7 expression is essential to restrict autoimmunity and dendritic cell proliferation
    Jonathan A Deane
    Laboratory of Immunogenetics, NIAID NIH, Rockville, MD 20852, USA
    Immunity 27:801-10. 2007
  4. ncbi request reprint A lupus-suppressor BALB/c locus restricts IgG2 autoantibodies without altering intrinsic B cell-tolerance mechanisms
    Tatyana Tarasenko
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    J Immunol 180:3807-14. 2008
  5. pmc Dual signaling by innate and adaptive immune receptors is required for TLR7-induced B-cell-mediated autoimmunity
    Elizabeth R Walsh
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 109:16276-81. 2012
  6. pmc Genetic susceptibility to systemic lupus erythematosus protects against cerebral malaria in mice
    Michael Waisberg
    Laboratories of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 108:1122-7. 2011
  7. pmc Ifih1 gene dose effect reveals MDA5-mediated chronic type I IFN gene signature, viral resistance, and accelerated autoimmunity
    Steve P Crampton
    Laboratory of Immunogenetics, National Institute of Allergic and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    J Immunol 188:1451-9. 2012
  8. pmc T cell-specific deletion of the inositol phosphatase SHIP reveals its role in regulating Th1/Th2 and cytotoxic responses
    Tatyana Tarasenko
    Laboratories of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 104:11382-7. 2007
  9. doi request reprint Aberrant antibody affinity selection in SHIP-deficient B cells
    Wai Hang Leung
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA
    Eur J Immunol 43:371-81. 2013
  10. pmc Differential roles for the inositol phosphatase SHIP in the regulation of macrophages and lymphocytes
    Wai Hang Leung
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12441 Parklawn Drive, Twinbrook 2, Room 217, Rockville, MD 20852, USA
    Immunol Res 43:243-51. 2009

Collaborators

Detail Information

Publications18

  1. pmc An innate path to human B cell tolerance
    Silvia Bolland
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Immunity 29:667-9. 2008
    ..Work by Isnardi et al. (2008) in this issue of Immunity suggests that removal of autoreactivity from the immature B cell pool also requires innate immunity pathways...
  2. pmc Vicious circle: systemic autoreactivity in Ro52/TRIM21-deficient mice
    Silvia Bolland
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville MD 20852, USA
    J Exp Med 206:1647-51. 2009
    ..The findings reveal that injury-induced systemic autoimmune disease is exacerbated in the absence of Ro52/Trim21 and is driven by the IL-23-Th17 pathway...
  3. pmc Control of toll-like receptor 7 expression is essential to restrict autoimmunity and dendritic cell proliferation
    Jonathan A Deane
    Laboratory of Immunogenetics, NIAID NIH, Rockville, MD 20852, USA
    Immunity 27:801-10. 2007
    ..These results underscore the importance of tightly regulating expression of TLR7 to prevent spontaneous triggering of harmful autoreactive and inflammatory responses...
  4. ncbi request reprint A lupus-suppressor BALB/c locus restricts IgG2 autoantibodies without altering intrinsic B cell-tolerance mechanisms
    Tatyana Tarasenko
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    J Immunol 180:3807-14. 2008
    ..Thus, sbb2(a) provides an example of a non-MHC lupus-suppressor locus that protects from disease by restricting the production of pathogenic IgG isotypes even in backgrounds with inefficient Ab editing checkpoints...
  5. pmc Dual signaling by innate and adaptive immune receptors is required for TLR7-induced B-cell-mediated autoimmunity
    Elizabeth R Walsh
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 109:16276-81. 2012
    ....
  6. pmc Genetic susceptibility to systemic lupus erythematosus protects against cerebral malaria in mice
    Michael Waisberg
    Laboratories of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 108:1122-7. 2011
    ....
  7. pmc Ifih1 gene dose effect reveals MDA5-mediated chronic type I IFN gene signature, viral resistance, and accelerated autoimmunity
    Steve P Crampton
    Laboratory of Immunogenetics, National Institute of Allergic and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    J Immunol 188:1451-9. 2012
    ..Thus, MDA5 transgenic mice provide evidence that chronic elevated levels of IFN-I are not sufficient to initiate autoimmunity or inflammation although they might exacerbate an ongoing autoimmune pathology...
  8. pmc T cell-specific deletion of the inositol phosphatase SHIP reveals its role in regulating Th1/Th2 and cytotoxic responses
    Tatyana Tarasenko
    Laboratories of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Proc Natl Acad Sci U S A 104:11382-7. 2007
    ..Overall our experiments indicate that in T cells SHIP negatively regulates cytokine-mediated activation in a way that allows effective Th2 responses and limits T cell cytotoxicity...
  9. doi request reprint Aberrant antibody affinity selection in SHIP-deficient B cells
    Wai Hang Leung
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA
    Eur J Immunol 43:371-81. 2013
    ..These results illustrate the importance of negative regulation of B-cell responses, as lower thresholds for B-cell activation promote survival of low affinity and deleterious receptors to the detriment of optimal Ab affinity maturation...
  10. pmc Differential roles for the inositol phosphatase SHIP in the regulation of macrophages and lymphocytes
    Wai Hang Leung
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12441 Parklawn Drive, Twinbrook 2, Room 217, Rockville, MD 20852, USA
    Immunol Res 43:243-51. 2009
    ..In this review we summarize our observations from mice with deletion of SHIP in lymphocyte and macrophage lineages and contrast them with earlier data gathered by the analysis of SHIP null mice...
  11. ncbi request reprint FcgammaRIIB as a modulator of autoimmune disease susceptibility
    Tatyana Tarasenko
    Autoimmunity and Functional Genomics Section, Laboratory of Immunogenetics, Rockville, MD 20852, USA
    Autoimmunity 40:409-17. 2007
    ..In this review we discuss how dysregulation of FcgammaRIIB can result in a lowered threshold for autoimmunity in mice and humans. We close with a discussion of the potential for applying these findings to immunotherapy...
  12. pmc Innate pathways to B-cell activation and tolerance
    Steve P Crampton
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA
    Ann N Y Acad Sci 1183:58-68. 2010
    ..We review here recent literature describing intrinsic and extrinsic effects of TLR stimulation on the fate of B cells, with particular attention to autoimmune diseases...
  13. ncbi request reprint Nucleic acid-sensing TLRs as modifiers of autoimmunity
    Jonathan A Deane
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    J Immunol 177:6573-8. 2006
    ..By considering the sources, localization, and expression of both nucleic acids and the molecules that bind them, we discuss several ways that innate immunity can play a role in the development of systemic autoimmunity...
  14. pmc Speckled-like pattern in the germinal center (SLIP-GC), a nuclear GTPase expressed in activation-induced deaminase-expressing lymphomas and germinal center B cells
    Kathleen Richter
    Laboratory of Molecular Genetics, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    J Biol Chem 284:30652-61. 2009
    ..These results strongly suggest that SLIP-GC is a replication-related protein in germinal center B cells whose reduction is toxic to cells through an AID-dependent mechanism...
  15. pmc The impact of genetic susceptibility to systemic lupus erythematosus on placental malaria in mice
    Michael Waisberg
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America
    PLoS ONE 8:e62820. 2013
    ..Thus, although SLE susceptibility was not protective in PM in mice it also did not have a negative impact on reproductive fitness...
  16. ncbi request reprint The inositol 5'-phosphatase SHIP-2 negatively regulates IgE-induced mast cell degranulation and cytokine production
    Wai Hang Leung
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12441 Parklawn Drive, Rockville, MD 20852, USA
    J Immunol 179:95-102. 2007
    ..Our results report a negative regulatory role of SHIP-2 on mast cell activation that is calcium independent and distinct from the regulation by SHIP-1...
  17. ncbi request reprint Autoreactive B cell responses to RNA-related antigens due to TLR7 gene duplication
    Prapaporn Pisitkun
    Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases NIAID, NIH, Rockville, MD 20852, USA
    Science 312:1669-72. 2006
    ..These results reveal high divergence in mouse Y chromosomes and represent a good example of gene copy number qualitatively altering a polygenic disease manifestation...
  18. ncbi request reprint The B cell inhibitory Fc receptor triggers apoptosis by a novel c-Abl family kinase-dependent pathway
    Shiang Jong Tzeng
    Laboratory of Immunogenetics, NIAID, National Institutes of Health, Rockville, Maryland 20852, USA
    J Biol Chem 280:35247-54. 2005
    ..These results define a novel Abl family kinase-dependent Fc gammaRIIB1 signaling pathway that functions independently of the BCR in controlling antigen-driven B cell responses...