James D Gorham

Summary

Affiliation: Dartmouth Medical School
Country: USA

Publications

  1. ncbi Transforming growth factor-beta1, Th1 responses, and autoimmune liver disease
    James D Gorham
    Department of Pathology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA
    Transfusion 45:51S-59S. 2005
  2. ncbi End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas
    Richard T Robinson
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 182:3278-84. 2009
  3. ncbi TGF-beta 1 regulates antigen-specific CD4+ T cell responses in the periphery
    Richard T Robinson
    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
    J Immunol 179:71-9. 2007
  4. ncbi TGF-beta1 inhibits T-bet induction by IFN-gamma in murine CD4+ T cells through the protein tyrosine phosphatase Src homology region 2 domain-containing phosphatase-1
    Il Kyoo Park
    Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 175:5666-74. 2005
  5. ncbi TGF-beta 1 inhibition of IFN-gamma-induced signaling and Th1 gene expression in CD4+ T cells is Smad3 independent but MAP kinase dependent
    Il Kyoo Park
    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
    Mol Immunol 44:3283-90. 2007
  6. ncbi TGF-beta 1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4+ T cells at priming and at recall: differential involvement of Stat4 and T-bet
    Jack T Lin
    Department of Microbiology and Immunology and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 174:5950-8. 2005
  7. ncbi Restriction of the CD4+ T-cell receptor repertoire prevents immune pathology in TGF-beta1 knockout mice
    Richard T Robinson
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Lab Invest 86:815-28. 2006
  8. ncbi Type 1 T helper cells induce the accumulation of myeloid-derived suppressor cells in the inflamed Tgfb1 knockout mouse liver
    James G Cripps
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Hepatology 52:1350-9. 2010
  9. ncbi MHC-independent genetic regulation of liver damage in a mouse model of autoimmune hepatocellular injury
    Jack T Lin
    Department of Microbiology and Immunology, The Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH 03756, USA
    Lab Invest 85:550-61. 2005
  10. ncbi The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis
    Michael W Milks
    Department of Pathology, Dartmouth Medical School, Dartmouth Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA
    Liver Int 29:1307-15. 2009

Collaborators

  • Jing Wang
  • Justin M M Cates
  • Michael L Whitfield
  • Ross M Kedl
  • Leonard D Shultz
  • J J Letterio
  • James P AuBuchon
  • Richard T Robinson
  • James G Cripps
  • Jack T Lin
  • Il Kyoo Park
  • Michael W Milks
  • Il-Kyoo Park
  • Cory L Ahonen
  • Tatsuro Yoshida
  • Tamar J Kitzmiller
  • Margaret A French
  • James L Sung
  • Lynnie A Rudner
  • Ian Blumenthal
  • Ann Maria
  • Todd A Pearson
  • Kathryn A English
  • Heping Lin
  • Jennifer L Sargent
  • Mark W Bitensky
  • Kevin Y Foster
  • Edward J Usherwood
  • Shinichiro Fuse
  • Arief A Suriawinata
  • Mary Jo Turk
  • Marc S Ernstoff
  • Sean C Gifford
  • Larry J Dumont
  • Anna Wasiuk
  • Randolph J Noelle
  • Stacey L Martin
  • Luxi Xia
  • Douglas M Franz
  • Elizabeth M Duncan
  • Hillary D White
  • Darci A Dyer

Detail Information

Publications15

  1. ncbi Transforming growth factor-beta1, Th1 responses, and autoimmune liver disease
    James D Gorham
    Department of Pathology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA
    Transfusion 45:51S-59S. 2005
    ..In this review, I summarize findings published or in press from our laboratory on disease pathogenesis in TGF-beta1-/- mice and then discuss some of the exciting (as-yet-unpublished) directions our laboratory is currently taking...
  2. ncbi End-organ damage in a mouse model of fulminant liver inflammation requires CD4+ T cell production of IFN-gamma but is independent of Fas
    Richard T Robinson
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 182:3278-84. 2009
    ....
  3. ncbi TGF-beta 1 regulates antigen-specific CD4+ T cell responses in the periphery
    Richard T Robinson
    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
    J Immunol 179:71-9. 2007
    ..These results indicate that CD4+ T cells in TGF-beta1(-/-) mice are activated by and respond to self-Ags present in the periphery, and define a key role for TGF-beta1 in the peripheral regulation of Ag-specific CD4+ T cell responses...
  4. ncbi TGF-beta1 inhibits T-bet induction by IFN-gamma in murine CD4+ T cells through the protein tyrosine phosphatase Src homology region 2 domain-containing phosphatase-1
    Il Kyoo Park
    Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 175:5666-74. 2005
    ..Together, these data show that TGF-beta1 suppresses IFN-gamma signaling and transcriptional responses in CD4+ T cells through the PTP Shp-1...
  5. ncbi TGF-beta 1 inhibition of IFN-gamma-induced signaling and Th1 gene expression in CD4+ T cells is Smad3 independent but MAP kinase dependent
    Il Kyoo Park
    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
    Mol Immunol 44:3283-90. 2007
    ..Thus, TGF-beta1's inhibition of IFN-gamma signaling in T cells is mediated through a highly specific Smad3 independent, MEK/ERK-dependent signaling pathway...
  6. ncbi TGF-beta 1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4+ T cells at priming and at recall: differential involvement of Stat4 and T-bet
    Jack T Lin
    Department of Microbiology and Immunology and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 174:5950-8. 2005
    ..These data show that TGF-beta1 uses distinct mechanisms to inhibit IFN-gamma expression in CD4(+) T cells at priming and at recall...
  7. ncbi Restriction of the CD4+ T-cell receptor repertoire prevents immune pathology in TGF-beta1 knockout mice
    Richard T Robinson
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Lab Invest 86:815-28. 2006
    ..Rather, T-cell activation and pathology in TGF-beta1-/- mice appear to be functions of typical TCR activation pathways. This supports the hypothesis that immune pathology in TGF-beta1-/- mice is self-antigen triggered...
  8. ncbi Type 1 T helper cells induce the accumulation of myeloid-derived suppressor cells in the inflamed Tgfb1 knockout mouse liver
    James G Cripps
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Hepatology 52:1350-9. 2010
    ..We propose that MDSCs serve an important negative feedback function in liver immune homeostasis, and that insufficient or inappropriate activity of this cell population may contribute to inflammatory liver pathology...
  9. ncbi MHC-independent genetic regulation of liver damage in a mouse model of autoimmune hepatocellular injury
    Jack T Lin
    Department of Microbiology and Immunology, The Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH 03756, USA
    Lab Invest 85:550-61. 2005
    ..This constitutes the first direct evidence that susceptibility to autoimmune hepatocellular damage, at least in mice, can be determined by genetic loci distinct from the MHC...
  10. ncbi The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis
    Michael W Milks
    Department of Pathology, Dartmouth Medical School, Dartmouth Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA
    Liver Int 29:1307-15. 2009
    ..These results provide a clearer understanding of the role of Ifng in the molecular basis of necroinflammatory liver disease...
  11. ncbi MDSC in autoimmunity
    James G Cripps
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Int Immunopharmacol 11:789-93. 2011
    ..A logical corollary of this hypothesis is that a failure of endogenous MDSC to appropriately control autoimmune T cell responses in vivo may actually contribute to the pathogenesis of autoimmune disease...
  12. ncbi Enhanced efficacy and reduced toxicity of multifactorial adjuvants compared with unitary adjuvants as cancer vaccines
    Cory L Ahonen
    Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA
    Blood 111:3116-25. 2008
    ..These findings provide intelligent strategies for the formulation of multifactorial vaccines to achieve maximal efficacy in cancer vaccine trials in humans...
  13. ncbi Necroinflammatory liver disease in BALB/c background, TGF-beta 1-deficient mice requires CD4+ T cells
    Lynnie A Rudner
    Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756, USA
    J Immunol 170:4785-92. 2003
    ..Furthermore, TGF-beta1 has a critical role in homeostatic regulation of the hepatic immune system, inhibiting the development or expansion of hepatic cytolytic CD4(+) T cells...
  14. ncbi CD28 co-stimulation regulates the effect of transforming growth factor-beta1 on the proliferation of naïve CD4+ T cells
    James L Sung
    Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
    Int Immunopharmacol 3:233-45. 2003
    ....
  15. ncbi The effects of additive solution pH and metabolic rejuvenation on anaerobic storage of red cells
    Tatsuro Yoshida
    Biomedical Engineering Department, Boston University College of Engineering, Boston, Massachusetts 02215, USA
    Transfusion 48:2096-105. 2008
    ..Our objective was to determine whether anaerobic storage with acidified additive solution (AS) coupled with metabolic rejuvenation might further improve the benefits of anaerobic storage...