P J Utz

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi The 72-kDa component of signal recognition particle is cleaved during apoptosis
    P J Utz
    Department of Medicine, Division of Rheumatology, Immunology, and Allergy, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 273:35362-70. 1998
  2. ncbi Monoclonal antibodies derived from BALB/c mice immunized with apoptotic Jurkat T cells recognize known autoantigens
    T J Gensler
    The Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA
    J Autoimmun 16:59-69. 2001
  3. ncbi Death, autoantigen modifications, and tolerance
    P J Utz
    Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    Arthritis Res 2:101-14. 2000
  4. ncbi Life and death decisions: regulation of apoptosis by proteolysis of signaling molecules
    P J Utz
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, Stanford, CA 94305, USA
    Cell Death Differ 7:589-602. 2000
  5. ncbi Multiplexed assays for identification of biomarkers and surrogate markers in systemic lupus erythematosus
    P J Utz
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    Lupus 13:304-11. 2004
  6. ncbi Detection of apoptosis-specific autoantibodies directed against granzyme B-induced cleavage fragments of the SS-B (La) autoantigen in sera from patients with primary Sjögren's syndrome
    M Huang
    First Department of Internal Medicine, Graduate School of Biochemical Sciences, Nagasaki University, Japan
    Clin Exp Immunol 142:148-54. 2005
  7. ncbi Autoantibodies in early arthritis: advances in diagnosis and prognostication
    W Hueber
    Department of Medicine, Division of Rheumatology and Immunology, Stanford University School of Medicine, Stanford, California, USA
    Clin Exp Rheumatol 21:S59-64. 2003
  8. ncbi Unlocking the "PAD" lock on rheumatoid arthritis
    P J Utz
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA
    Ann Rheum Dis 63:330-2. 2004
  9. ncbi Suppression of autoimmunity via microbial mimics of altered peptide ligands
    L Steinman
    Dept of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine B002, Stanford University School of Medicine, CA 94305, USA
    Curr Top Microbiol Immunol 296:55-63. 2005

Collaborators

Detail Information

Publications9

  1. ncbi The 72-kDa component of signal recognition particle is cleaved during apoptosis
    P J Utz
    Department of Medicine, Division of Rheumatology, Immunology, and Allergy, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 273:35362-70. 1998
    ..The 72-kDa component of the SRP joins a growing list of autoantigens that undergo post-translational modifications during programmed cell death...
  2. ncbi Monoclonal antibodies derived from BALB/c mice immunized with apoptotic Jurkat T cells recognize known autoantigens
    T J Gensler
    The Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA
    J Autoimmun 16:59-69. 2001
    ..These findings are consistent with the hypothesis that apoptosis can contribute to the development of autoimmunity...
  3. ncbi Death, autoantigen modifications, and tolerance
    P J Utz
    Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    Arthritis Res 2:101-14. 2000
    ..This review will address the potential role played by death-specific modifications of autoantigens in bypassing tolerance to highly conserved autoantigens, including nucleic acids, lipids, and proteins...
  4. ncbi Life and death decisions: regulation of apoptosis by proteolysis of signaling molecules
    P J Utz
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, Stanford, CA 94305, USA
    Cell Death Differ 7:589-602. 2000
    ..By acting as executioners and as important 'molecular sensors' of the degree of cellular injury, the signaling proteins described in this review are strong candidates to mediate downstream events, both in condemned and in viable cells...
  5. ncbi Multiplexed assays for identification of biomarkers and surrogate markers in systemic lupus erythematosus
    P J Utz
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    Lupus 13:304-11. 2004
    ..Their potential and pitfalls for monitoring patients with SLE, particularly those enrolled in clinical trials testing novel therapeutics, will be discussed...
  6. ncbi Detection of apoptosis-specific autoantibodies directed against granzyme B-induced cleavage fragments of the SS-B (La) autoantigen in sera from patients with primary Sjögren's syndrome
    M Huang
    First Department of Internal Medicine, Graduate School of Biochemical Sciences, Nagasaki University, Japan
    Clin Exp Immunol 142:148-54. 2005
    ..This is the first report describing autoantibodies in sera from primary SS patients that specifically recognize fragments of the La protein that are produced by the granzyme B protease...
  7. ncbi Autoantibodies in early arthritis: advances in diagnosis and prognostication
    W Hueber
    Department of Medicine, Division of Rheumatology and Immunology, Stanford University School of Medicine, Stanford, California, USA
    Clin Exp Rheumatol 21:S59-64. 2003
    ....
  8. ncbi Unlocking the "PAD" lock on rheumatoid arthritis
    P J Utz
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA
    Ann Rheum Dis 63:330-2. 2004
  9. ncbi Suppression of autoimmunity via microbial mimics of altered peptide ligands
    L Steinman
    Dept of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine B002, Stanford University School of Medicine, CA 94305, USA
    Curr Top Microbiol Immunol 296:55-63. 2005
    ..Autoimmunity could therefore be modulated via microbial immunity, which may account for relapse and remission of ongoing disease...