Joel N H Stern

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. doi request reprint Molecular signatures distinguishing active from latent tuberculosis in peripheral blood mononuclear cells, after in vitro antigenic stimulation with purified protein derivative of tuberculin (PPD) or Candida: a preliminary report
    Joel N H Stern
    Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Immunol Res 45:1-12. 2009
  2. doi request reprint Strategies for the identification of loci responsible for the pathogenesis of multiple sclerosis
    Joel N H Stern
    Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 190 Longwood Ave, Boston, MA, USA
    Cell Mol Biol Lett 13:656-66. 2008
  3. pmc Amino acid copolymer-specific IL-10-secreting regulatory T cells that ameliorate autoimmune diseases in mice
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 105:5172-6. 2008
  4. pmc Promoting tolerance to proteolipid protein-induced experimental autoimmune encephalomyelitis through targeting dendritic cells
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 107:17280-5. 2010
  5. pmc Amelioration of proteolipid protein 139-151-induced encephalomyelitis in SJL mice by modified amino acid copolymers and their mechanisms
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 101:11743-8. 2004
  6. ncbi request reprint Copolymer effects on microglia and T cells in the central nervous system of humanized mice
    Zsolt Illes
    Center for Neurological Diseases, Harvard Institutes of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02138, USA
    Eur J Immunol 35:3683-93. 2005
  7. pmc Modified amino acid copolymers suppress myelin basic protein 85-99-induced encephalomyelitis in humanized mice through different effects on T cells
    Zsolt Illes
    Center for Neurologic Diseases, Harvard Institute of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:11749-54. 2004
  8. pmc Peptide 15-mers of defined sequence that substitute for random amino acid copolymers in amelioration of experimental autoimmune encephalomyelitis
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 102:1620-5. 2005
  9. doi request reprint The autoimmune TCR-Ob.2F3 can bind to MBP85-99/HLA-DR2 having an unconventional mode as in TCR-Ob.1A12
    Zenichiro Kato
    Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02193, USA
    Mol Immunol 48:314-20. 2010
  10. pmc T cell receptors in an IL-10-secreting amino acid copolymer-specific regulatory T cell line that mediates bystander immunosuppression
    Hong Zhang
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 106:3336-41. 2009

Collaborators

Detail Information

Publications20

  1. doi request reprint Molecular signatures distinguishing active from latent tuberculosis in peripheral blood mononuclear cells, after in vitro antigenic stimulation with purified protein derivative of tuberculin (PPD) or Candida: a preliminary report
    Joel N H Stern
    Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Immunol Res 45:1-12. 2009
    ....
  2. doi request reprint Strategies for the identification of loci responsible for the pathogenesis of multiple sclerosis
    Joel N H Stern
    Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 190 Longwood Ave, Boston, MA, USA
    Cell Mol Biol Lett 13:656-66. 2008
    ..We review these developments, advances in technology and discuss recent results in this article...
  3. pmc Amino acid copolymer-specific IL-10-secreting regulatory T cells that ameliorate autoimmune diseases in mice
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 105:5172-6. 2008
    ..e., PLP139-151(EAE), MBP85-99 (EAE), and bovine peripheral nerve myelin (experimental autoimmune neuritis), indicating they function by bystander suppression...
  4. pmc Promoting tolerance to proteolipid protein-induced experimental autoimmune encephalomyelitis through targeting dendritic cells
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 107:17280-5. 2010
    ..In addition, evidence for a CD4(+) T cell-mediated suppressor mechanism was obtained...
  5. pmc Amelioration of proteolipid protein 139-151-induced encephalomyelitis in SJL mice by modified amino acid copolymers and their mechanisms
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 101:11743-8. 2004
    ....
  6. ncbi request reprint Copolymer effects on microglia and T cells in the central nervous system of humanized mice
    Zsolt Illes
    Center for Neurological Diseases, Harvard Institutes of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02138, USA
    Eur J Immunol 35:3683-93. 2005
    ....
  7. pmc Modified amino acid copolymers suppress myelin basic protein 85-99-induced encephalomyelitis in humanized mice through different effects on T cells
    Zsolt Illes
    Center for Neurologic Diseases, Harvard Institute of Medicine, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:11749-54. 2004
    ..Thus, copolymers generated by using different amino acids inhibited disease using different mechanisms to regulate T cell responses...
  8. pmc Peptide 15-mers of defined sequence that substitute for random amino acid copolymers in amelioration of experimental autoimmune encephalomyelitis
    Joel N H Stern
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 102:1620-5. 2005
    ..These peptide 15-mers provide specific, nonrandom sequences that appear to be at least as effective as random copolymers in suppressing EAE in several models...
  9. doi request reprint The autoimmune TCR-Ob.2F3 can bind to MBP85-99/HLA-DR2 having an unconventional mode as in TCR-Ob.1A12
    Zenichiro Kato
    Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02193, USA
    Mol Immunol 48:314-20. 2010
    ....
  10. pmc T cell receptors in an IL-10-secreting amino acid copolymer-specific regulatory T cell line that mediates bystander immunosuppression
    Hong Zhang
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 106:3336-41. 2009
    ..These data lead to a hypothesis regarding the origin of the epigenetic modifications that lead to selective cytokine secretion in T cells...
  11. pmc Positioning of autoimmune TCR-Ob.2F3 and TCR-Ob.3D1 on the MBP85-99/HLA-DR2 complex
    Zenichiro Kato
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 105:15523-8. 2008
    ..Two of them are located near the N terminus of the peptide-binding cleft, whereas the third is near the center. These data are compatible with the hypothesis that the rotation of the TCRs may alter the downstream signaling...
  12. ncbi request reprint Interaction of KIR genes and G1M immunoglobulin allotypes confer susceptibility to type 2 diabetes in Puerto Rican Americans
    Joaquin Zuniga
    Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Hum Immunol 67:907-14. 2006
    ..Our findings are important for understanding the autoimmune or innate immune inflammatory-mediated mechanisms involved in the pathogenesis of T2D...
  13. pmc JNK MAP kinase activation is required for MTOC and granule polarization in NKG2D-mediated NK cell cytotoxicity
    Changlin Li
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 105:3017-22. 2008
    ..Thus, activation of two MAP kinase pathways is required for cytotoxic granule and MTOC polarization and for cytotoxicity of human NK cells when NKG2D is ligated...
  14. doi request reprint A review of the current use of rituximab in autoimmune diseases
    Hakan M Gürcan
    Center for Blistering Diseases, New England Baptist Hospital, Boston, MA 02120, USA
    Int Immunopharmacol 9:10-25. 2009
    ..In patients with autoimmune diseases the incidence of serious and severe side effects is low. Systemic infection still remains a major concern and may result in death...
  15. pmc Novel synthetic amino acid copolymers that inhibit autoantigen-specific T cell responses and suppress experimental autoimmune encephalomyelitis
    Masha Fridkis-Hareli
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA
    J Clin Invest 109:1635-43. 2002
    ..Thus, random synthetic copolymers designed according to the binding motif of the human immunodominant epitope MBP 85-99 and the binding pockets of HLA-DR2 might be more beneficial than Cop 1 in treatment of MS...
  16. doi request reprint Cytokine profiles in pemphigus vulgaris patients treated with intravenous immunoglobulins as compared to conventional immunosuppressive therapy
    Derin B Keskin
    Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA, USA
    Cytokine 41:315-21. 2008
    ..The conclusions from this limited number of patients, prospectively studied, would suggest that both CIST and IVIg therapies are similar in their ability to influence a panel of cytokines in patients with pemphigus vulgaris...
  17. pmc Circulating microparticles: square the circle
    Natasha S Barteneva
    Program in Cellular and Molecular Medicine, Boston Children s Hospital, D 249, 200 Longwood Avenue, Boston, MA 02115, USA
    BMC Cell Biol 14:23. 2013
    ..The present review summarizes current knowledge about microparticles (MPs) and provides a systematic overview of last 20 years of research on circulating MPs, with particular focus on their clinical relevance...
  18. pmc TGFbeta promotes conversion of CD16+ peripheral blood NK cells into CD16- NK cells with similarities to decidual NK cells
    Derin B Keskin
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Proc Natl Acad Sci U S A 104:3378-83. 2007
    ..These progenitors also produced NK cells when cultured in conditioned medium from decidual stromal cells supplemented with IL-15 and stem cell factor...
  19. pmc Developmental bias in cleavage-stage mouse blastomeres
    Inna Tabansky
    The Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA
    Curr Biol 23:21-31. 2013
    ..To determine whether blastomere allocation to the two earliest lineages is random, we developed and utilized a recombination-mediated, noninvasive combinatorial fluorescent labeling method for embryonic lineage tracing...
  20. pmc VAMP4- and VAMP7-expressing vesicles are both required for cytotoxic granule exocytosis in NK cells
    Konrad Krzewski
    Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA
    Eur J Immunol 41:3323-9. 2011
    ..Furthermore, VAMP7 but not VAMP4 is involved in IFN-γ secretion in NK cells, indicating that VAMP7 is involved in many fusion processes and thus plays a more general function in NK-cell activity than VAMP4...