S A Huber

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. pmc Hormonal regulation of CD4(+) T-cell responses in coxsackievirus B3-induced myocarditis in mice
    S A Huber
    Departments of Pathology and Medicine, University of Vermont, Burlington, Vermont 05405, USA
    J Virol 73:4689-95. 1999
  2. pmc gamma delta+ T cells regulate major histocompatibility complex class II(IA and IE)-dependent susceptibility to coxsackievirus B3-induced autoimmune myocarditis
    S A Huber
    Department of Pathology, Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405, USA
    J Virol 73:5630-6. 1999
  3. pmc Cytokine production by Vgamma(+)-T-cell subsets is an important factor determining CD4(+)-Th-cell phenotype and susceptibility of BALB/c mice to coxsackievirus B3-induced myocarditis
    S A Huber
    Department of Pathology, University of Vermont, Burlington, Vermont, USA
    J Virol 75:5860-9. 2001
  4. ncbi request reprint V gamma 1+ T cells suppress and V gamma 4+ T cells promote susceptibility to coxsackievirus B3-induced myocarditis in mice
    S A Huber
    Department of Pathology, University of Vermont, Burlington, VT 05446, USA
    J Immunol 165:4174-81. 2000
  5. ncbi request reprint T helper-cell phenotype regulates atherosclerosis in mice under conditions of mild hypercholesterolemia
    S A Huber
    Department of Pathology, University of Vermont, Burlington, USA
    Circulation 103:2610-6. 2001
  6. pmc Coxsackievirus B3-induced myocarditis: infection of females during the estrus phase of the ovarian cycle leads to activation of T regulatory cells
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Drive, Suite 2, Colchester, Vermont 05446, USA
    Virology 378:292-8. 2008
  7. pmc Coxsackievirus B3 induction of NFAT: requirement for myocarditis susceptibility
    S A Huber
    Department of Pathology, University of Vermont, Colchester, VT 05446, USA
    Virology 381:155-60. 2008
  8. ncbi request reprint CD1d expression on hemopoietic cells promotes CD4+ Th1 response in coxsackievirus B3 induced myocarditis
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Drive, Suite 2, Burlington, VT 05446, USA
    Virology 352:226-36. 2006
  9. pmc Vgamma4(+) T cells promote autoimmune CD8(+) cytolytic T-lymphocyte activation in coxsackievirus B3-induced myocarditis in mice: role for CD4(+) Th1 cells
    S A Huber
    Department of Pathology, University of Vermont, Burlington, Vermont, USA
    J Virol 76:10785-90. 2002
  10. pmc Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Dr, Suite 2, Colchester, VT 05446, USA
    J Virol 79:2659-65. 2005

Collaborators

Detail Information

Publications17

  1. pmc Hormonal regulation of CD4(+) T-cell responses in coxsackievirus B3-induced myocarditis in mice
    S A Huber
    Departments of Pathology and Medicine, University of Vermont, Burlington, Vermont 05405, USA
    J Virol 73:4689-95. 1999
    ..Taken together, our results indicate that testosterone promotes a CD4(+) Th1 cell response and myocarditis by promoting increased gammadelta+ cell activation...
  2. pmc gamma delta+ T cells regulate major histocompatibility complex class II(IA and IE)-dependent susceptibility to coxsackievirus B3-induced autoimmune myocarditis
    S A Huber
    Department of Pathology, Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405, USA
    J Virol 73:5630-6. 1999
    ....
  3. pmc Cytokine production by Vgamma(+)-T-cell subsets is an important factor determining CD4(+)-Th-cell phenotype and susceptibility of BALB/c mice to coxsackievirus B3-induced myocarditis
    S A Huber
    Department of Pathology, University of Vermont, Burlington, Vermont, USA
    J Virol 75:5860-9. 2001
    ..The cytokines produced by the Vgamma subpopulation have a significant influence on the CD4(+)-Th-cell phenotype...
  4. ncbi request reprint V gamma 1+ T cells suppress and V gamma 4+ T cells promote susceptibility to coxsackievirus B3-induced myocarditis in mice
    S A Huber
    Department of Pathology, University of Vermont, Burlington, VT 05446, USA
    J Immunol 165:4174-81. 2000
    ..Th subset analysis suggests that Vgamma1(+) cells biased the CD4(+) T cells to a dominant Th2 cell response, whereas Vgamma4(+) cells biased CD4(+) T cells toward a dominant Th1 cell response...
  5. ncbi request reprint T helper-cell phenotype regulates atherosclerosis in mice under conditions of mild hypercholesterolemia
    S A Huber
    Department of Pathology, University of Vermont, Burlington, USA
    Circulation 103:2610-6. 2001
    ..T cells are implicated in atherosclerosis, but little is known about the genetic control or molecular pathways, especially under conditions of mild hypercholesterolemia...
  6. pmc Coxsackievirus B3-induced myocarditis: infection of females during the estrus phase of the ovarian cycle leads to activation of T regulatory cells
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Drive, Suite 2, Colchester, Vermont 05446, USA
    Virology 378:292-8. 2008
    ..These results demonstrate that hormonal fluctuations occurring in normally cycling females can determine T regulatory cell response and control virus-induced pathogenesis...
  7. pmc Coxsackievirus B3 induction of NFAT: requirement for myocarditis susceptibility
    S A Huber
    Department of Pathology, University of Vermont, Colchester, VT 05446, USA
    Virology 381:155-60. 2008
    ..FasL expression by V gamma 4+ cells was also suppressed. Inhibition of FasL expression by V gamma 4+ cells is consistent with myocarditis protection in dnNFAT mice...
  8. ncbi request reprint CD1d expression on hemopoietic cells promotes CD4+ Th1 response in coxsackievirus B3 induced myocarditis
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Drive, Suite 2, Burlington, VT 05446, USA
    Virology 352:226-36. 2006
    ..These results show that Vgamma4+ cells modulate developing adaptive immunity through recognition of CD1d on CD4+ T cells, and that this interaction, more than Vgamma4+ cell interaction with infected cardiocytes, determines pathogenicity...
  9. pmc Vgamma4(+) T cells promote autoimmune CD8(+) cytolytic T-lymphocyte activation in coxsackievirus B3-induced myocarditis in mice: role for CD4(+) Th1 cells
    S A Huber
    Department of Pathology, University of Vermont, Burlington, Vermont, USA
    J Virol 76:10785-90. 2002
    ..Vgamma4(+) cells enhance CD4(+) Th1 (IFN-gamma(+)) cell activation through IFN-gamma- and CD1-dependent mechanisms. CD4(+) Th1 cells promote activation of the autoimmune CD8(+) alphabeta TCR(+) effectors...
  10. pmc Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis
    S A Huber
    University of Vermont, Department of Pathology, 208 South Park Dr, Suite 2, Colchester, VT 05446, USA
    J Virol 79:2659-65. 2005
    ..TNF-alpha treatment of uninfected endothelial cells had only a modest effect on CD1d expression, suggesting that optimal CD1d upregulation requires both infection and TNF-alpha signaling...
  11. pmc Differential Th1 and Th2 cell responses in male and female BALB/c mice infected with coxsackievirus group B type 3
    S A Huber
    Department of Pathology, University of Vermont, Burlington 05405
    J Virol 68:5126-32. 1994
    ..Treatment of the female donors with monoclonal antibodies to either CD3, CD4, or IL-4 molecules abrogates suppression...
  12. ncbi request reprint Dual functions of murine gammadelta cells in inflammation and autoimmunity in coxsackievirus B3-induced myocarditis: role of Vgamma1+ and Vgamma4+ cells
    S A Huber
    Department of Pathology, University of Vermont, Burlington, VT, USA
    Microbes Infect 7:537-43. 2005
    ..The CD4+ Th1 response is necessary for activation of the autoimmune CD8+ T cells, which kill uninfected cardiocytes through perforin-dependent mechanisms...
  13. ncbi request reprint T cells expressing the gamma delta T cell receptor induce apoptosis in cardiac myocytes
    S A Huber
    Department of Pathology, University of Vermont, Colchester 05446, USA
    Cardiovasc Res 45:579-87. 2000
    ..The objective of the present studies is to demonstrate that gamma delta T cells directly induce greater Fas-dependent apoptosis of cultured myocytes than T cells expressing the alpha beta TcR...
  14. ncbi request reprint Does the oxidative/glycolytic ratio determine proliferation or death in immune recognition?
    M K Newell
    Department of Medicine, University of Vermont College of Medicine, Burlington 05405, USA
    Ann N Y Acad Sci 887:77-82. 1999
    ..Thus, immune recognition can induce metabolic deviation. Metabolic deviation can result in altered immune recognition and ultimately in cell proliferation, cell differentiation, or cell death...
  15. ncbi request reprint Interleukin-6 exacerbates early atherosclerosis in mice
    S A Huber
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    Arterioscler Thromb Vasc Biol 19:2364-7. 1999
    ....
  16. ncbi request reprint Depletion of a gamma delta T cell subset can increase host resistance to a bacterial infection
    R L O'Brien
    Department of Immunology, National Jewish Medical and Research Center, Denver, CO 80206, USA
    J Immunol 165:6472-9. 2000
    ..Our findings indicate that Vgamma1(+) gammadelta T cells reduce the ability of the innate immune system to destroy Listeria, even though other gammadelta T cells as a whole promote clearance of this pathogen...
  17. ncbi request reprint Endogenous versus exogenous fatty acid availability affects lysosomal acidity and MHC class II expression
    S C Schweitzer
    Colorado University Institute of Bioenergetics, University of Colorado, Colorado Springs, CO, USA
    J Lipid Res 47:2525-37. 2006
    ..Collectively, these data demonstrate a mechanistic link between lipid availability and early events in the immune response...