Thomas Rauen

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc cAMP-responsive element modulator (CREM)α protein induces interleukin 17A expression and mediates epigenetic alterations at the interleukin-17A gene locus in patients with systemic lupus erythematosus
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:43437-46. 2011
  2. pmc cAMP responsive element modulator (CREM) α mediates chromatin remodeling of CD8 during the generation of CD3+ CD4- CD8- T cells
    Christian M Hedrich
    From the Department of Medicine, Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115
    J Biol Chem 289:2361-70. 2014
  3. pmc cAMP-responsive element modulator α (CREMα) contributes to decreased Notch-1 expression in T cells from patients with active systemic lupus erythematosus (SLE)
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 287:42525-32. 2012
  4. pmc cAMP response element modulator α controls IL2 and IL17A expression during CD4 lineage commitment and subset distribution in lupus
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:16606-11. 2012
  5. pmc CD3-T cell receptor co-stimulation through SLAMF3 and SLAMF6 receptors enhances RORγt recruitment to the IL17A promoter in human T lymphocytes
    Madhumouli Chatterjee
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess MedicalCenter, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 287:38168-77. 2012
  6. pmc cAMP-responsive element modulator α (CREMα) trans-represses the transmembrane glycoprotein CD8 and contributes to the generation of CD3+CD4-CD8- T cells in health and disease
    Christian M Hedrich
    From the Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115
    J Biol Chem 288:31880-7. 2013
  7. pmc cAMP responsive element modulator: a critical regulator of cytokine production
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Trends Mol Med 19:262-9. 2013
  8. pmc cAMP-responsive element modulator α (CREMα) suppresses IL-17F protein expression in T lymphocytes from patients with systemic lupus erythematosus (SLE)
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 287:4715-25. 2012
  9. pmc cAMP-responsive element modulator (CREM)α protein signaling mediates epigenetic remodeling of the human interleukin-2 gene: implications in systemic lupus erythematosus
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:43429-36. 2011
  10. pmc Cutting edge: Calcium/Calmodulin-dependent protein kinase type IV is essential for mesangial cell proliferation and lupus nephritis
    Kunihiro Ichinose
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 187:5500-4. 2011

Collaborators

Detail Information

Publications13

  1. pmc cAMP-responsive element modulator (CREM)α protein induces interleukin 17A expression and mediates epigenetic alterations at the interleukin-17A gene locus in patients with systemic lupus erythematosus
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:43437-46. 2011
    ..Our findings demonstrate an extended role for CREMα in the immunopathogenesis of SLE because it contributes to increased expression of IL-17A...
  2. pmc cAMP responsive element modulator (CREM) α mediates chromatin remodeling of CD8 during the generation of CD3+ CD4- CD8- T cells
    Christian M Hedrich
    From the Department of Medicine, Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115
    J Biol Chem 289:2361-70. 2014
    ..Thus, we propose that CREMα is essential for the expansion of double negative T cells in SLE. CREMα blockade may have therapeutic value in autoimmune disorders with DN T cell expansion. ..
  3. pmc cAMP-responsive element modulator α (CREMα) contributes to decreased Notch-1 expression in T cells from patients with active systemic lupus erythematosus (SLE)
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 287:42525-32. 2012
    ..Our data suggest a role for Notch-1 in SLE immunopathogenesis, and for the first time, we present molecular mechanisms that mediate dysregulated Notch-1 expression in SLE T cells...
  4. pmc cAMP response element modulator α controls IL2 and IL17A expression during CD4 lineage commitment and subset distribution in lupus
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:16606-11. 2012
    ..We conclude that CREMα mediates epigenetic remodeling of the IL2 and IL17A gene during T-cell differentiation in favor of effector memory T cells in health and disease...
  5. pmc CD3-T cell receptor co-stimulation through SLAMF3 and SLAMF6 receptors enhances RORγt recruitment to the IL17A promoter in human T lymphocytes
    Madhumouli Chatterjee
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess MedicalCenter, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 287:38168-77. 2012
    ..Thus, we have identified an additional mechanism that may be central for the specific control of IL17A gene regulation in systemic lupus erythematosus T lymphocytes...
  6. pmc cAMP-responsive element modulator α (CREMα) trans-represses the transmembrane glycoprotein CD8 and contributes to the generation of CD3+CD4-CD8- T cells in health and disease
    Christian M Hedrich
    From the Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115
    J Biol Chem 288:31880-7. 2013
    ..Therefore, CREMα represents a promising candidate in the search for biomarkers and treatment options in diseases in which double-negative T cells contribute to the pathogenesis. ..
  7. pmc cAMP responsive element modulator: a critical regulator of cytokine production
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Trends Mol Med 19:262-9. 2013
    ..We emphasize CREMα as a key molecule that drives autoimmunity...
  8. pmc cAMP-responsive element modulator α (CREMα) suppresses IL-17F protein expression in T lymphocytes from patients with systemic lupus erythematosus (SLE)
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 287:4715-25. 2012
    ..An increased IL-17A/IL-17F ratio may aggravate the proinflammatory phenotype of SLE...
  9. pmc cAMP-responsive element modulator (CREM)α protein signaling mediates epigenetic remodeling of the human interleukin-2 gene: implications in systemic lupus erythematosus
    Christian M Hedrich
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:43429-36. 2011
    ..For the first time, we provide direct evidence that CREMα mediates silencing of the IL2 gene in SLE T cells though histone deacetylation and CpG-DNA methylation...
  10. pmc Cutting edge: Calcium/Calmodulin-dependent protein kinase type IV is essential for mesangial cell proliferation and lupus nephritis
    Kunihiro Ichinose
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 187:5500-4. 2011
    ....
  11. pmc A novel intronic cAMP response element modulator (CREM) promoter is regulated by activator protein-1 (AP-1) and accounts for altered activation-induced CREM expression in T cells from patients with systemic lupus erythematosus
    Thomas Rauen
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:32366-72. 2011
    ..Our findings extend the understanding of CREM gene regulation in the context of T cell activation and disclose another difference in the transcriptional machinery in SLE T cells...
  12. pmc Increased expression of SLAM receptors SLAMF3 and SLAMF6 in systemic lupus erythematosus T lymphocytes promotes Th17 differentiation
    Madhumouli Chatterjee
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 188:1206-12. 2012
    ....
  13. pmc Transcriptional activation of the cAMP-responsive modulator promoter in human T cells is regulated by protein phosphatase 2A-mediated dephosphorylation of SP-1 and reflects disease activity in patients with systemic lupus erythematosus
    Yuang Taung Juang
    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 286:1795-801. 2011
    ..More importantly, CREM promoter activity mirrors reliably disease activity in SLE patients, underscoring its potential role as a biomarker for the prediction of flares in SLE patients...