Ralph C Budd

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. ncbi request reprint Cellular FLIP (long form) regulates CD8+ T cell activation through caspase-8-dependent NF-kappa B activation
    Austin Dohrman
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 174:5270-8. 2005
  2. pmc Death receptors couple to both cell proliferation and apoptosis
    Ralph C Budd
    Division of Immunobiology, Department of Medicine, Given Medical Building, D 305, The University of Vermont College of Medicine, Burlington, Vermont 05405 0068, USA
    J Clin Invest 109:437-41. 2002
  3. ncbi request reprint Cellular FLIP long form augments caspase activity and death of T cells through heterodimerization with and activation of caspase-8
    Austin Dohrman
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 175:311-8. 2005
  4. ncbi request reprint Augmentation of proliferation of vascular smooth muscle cells by plasminogen activator inhibitor type 1
    Yabing Chen
    Department of Medicine and Cardiovascular Research Institute, University of Vermont, Burlington, USA
    Arterioscler Thromb Vasc Biol 26:1777-83. 2006
  5. pmc Activation of gamma delta T cells by Borrelia burgdorferi is indirect via a TLR- and caspase-dependent pathway
    Cheryl Collins
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 50405, USA
    J Immunol 181:2392-8. 2008
  6. pmc Fas ligand deficiency impairs host inflammatory response against infection with the spirochete Borrelia burgdorferi
    Cuixia Shi
    Immunobiology Program, The University of Vermont College of Medicine, Given Medical Building, Burlington, VT 05405 0068, USA
    Infect Immun 74:1156-60. 2006
  7. ncbi request reprint Lyme arthritis synovial gammadelta T cells instruct dendritic cells via fas ligand
    Cheryl Collins
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 50405, USA
    J Immunol 175:5656-65. 2005
  8. pmc c-FLIP(S) reduces activation of caspase and NF-kappaB pathways and decreases T cell survival
    Jennifer Hinshaw-Makepeace
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Eur J Immunol 38:54-63. 2008
  9. pmc Reduced immune response to Borrelia burgdorferi in the absence of γδ T cells
    Cuixia Shi
    Vermont Center for Immunology and Infectious Diseases, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Infect Immun 79:3940-6. 2011
  10. ncbi request reprint Caspase-8 and c-FLIPL associate in lipid rafts with NF-kappaB adaptors during T cell activation
    Ravi S Misra
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405 0068, USA
    J Biol Chem 282:19365-74. 2007

Collaborators

Detail Information

Publications35

  1. ncbi request reprint Cellular FLIP (long form) regulates CD8+ T cell activation through caspase-8-dependent NF-kappa B activation
    Austin Dohrman
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 174:5270-8. 2005
    ..This provides a partial explanation of why caspase activity is required to initiate proliferation of resting T cells...
  2. pmc Death receptors couple to both cell proliferation and apoptosis
    Ralph C Budd
    Division of Immunobiology, Department of Medicine, Given Medical Building, D 305, The University of Vermont College of Medicine, Burlington, Vermont 05405 0068, USA
    J Clin Invest 109:437-41. 2002
  3. ncbi request reprint Cellular FLIP long form augments caspase activity and death of T cells through heterodimerization with and activation of caspase-8
    Austin Dohrman
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 175:311-8. 2005
    ..c-FLIP(L) is thus not only an inhibitor of cell death by Fas, it can also act as a principal activator of caspases independently of Fas...
  4. ncbi request reprint Augmentation of proliferation of vascular smooth muscle cells by plasminogen activator inhibitor type 1
    Yabing Chen
    Department of Medicine and Cardiovascular Research Institute, University of Vermont, Burlington, USA
    Arterioscler Thromb Vasc Biol 26:1777-83. 2006
    ..Because apoptosis and proliferation appear to be linked, we sought to determine whether increased PAI-1 would affect VSMC proliferation...
  5. pmc Activation of gamma delta T cells by Borrelia burgdorferi is indirect via a TLR- and caspase-dependent pathway
    Cheryl Collins
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 50405, USA
    J Immunol 181:2392-8. 2008
    ..Furthermore, B. burgdorferi stimulation of monocytes via TLR, and secondary activation of gammadelta T cells, are both caspase-dependent...
  6. pmc Fas ligand deficiency impairs host inflammatory response against infection with the spirochete Borrelia burgdorferi
    Cuixia Shi
    Immunobiology Program, The University of Vermont College of Medicine, Given Medical Building, Burlington, VT 05405 0068, USA
    Infect Immun 74:1156-60. 2006
    ..In addition, C3Hgld mice developed a greatly reduced incidence and severity of arthritis. The findings document a contribution of FasL to the host inflammatory response to B. burgdorferi...
  7. ncbi request reprint Lyme arthritis synovial gammadelta T cells instruct dendritic cells via fas ligand
    Cheryl Collins
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 50405, USA
    J Immunol 175:5656-65. 2005
    ..They also underscore the view that as levels of c-FLIP increase, Fas signaling can be diverted from induction of apoptosis to pathways leading to cell effector function...
  8. pmc c-FLIP(S) reduces activation of caspase and NF-kappaB pathways and decreases T cell survival
    Jennifer Hinshaw-Makepeace
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Eur J Immunol 38:54-63. 2008
    ..Consequently, T cells from c-FLIP(S)-transgenic mice undergo more rapid cell death both spontaneously and after activation. The findings suggest that c-FLIP(S) functions to reduce the expansion of T cells during an immune response...
  9. pmc Reduced immune response to Borrelia burgdorferi in the absence of γδ T cells
    Cuixia Shi
    Vermont Center for Immunology and Infectious Diseases, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Infect Immun 79:3940-6. 2011
    ..This paralleled a greater Borrelia burden in γδ-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of γδ T cells functioning to promote the adaptive immune response during infection...
  10. ncbi request reprint Caspase-8 and c-FLIPL associate in lipid rafts with NF-kappaB adaptors during T cell activation
    Ravi S Misra
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405 0068, USA
    J Biol Chem 282:19365-74. 2007
    ..The current findings define a link among TCR, caspases, and the NF-kappaB pathway that occurs in a sequestered lipid raft environment in T cells...
  11. ncbi request reprint Proteolytic regulation of nuclear factor of activated T (NFAT) c2 cells and NFAT activity by caspase-3
    Wenfang Wu
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, Vermont 05405, USA
    J Biol Chem 281:10682-90. 2006
    ..Our findings reveal a new post-transcriptional regulation of NFATc2 that operates, not only during apoptosis, but also in non-apoptotic effector T cells...
  12. pmc Increased caspase activity primes human Lyme arthritis synovial γδ T cells for proliferation and death
    Phan T Thai
    Vermont Center for Immunology and Infectious Diseases, University of Vermont College of Medicine, Burlington, VT 05405, USA
    Hum Immunol 72:1168-75. 2011
    ..Our current findings thus are consistent with a model in which human γδ T cells evolved to function quickly and transiently in an innate fashion...
  13. pmc Apoptosis regulators Fas and Bim synergistically control T-lymphocyte homeostatic proliferation
    Karen A Fortner
    Vermont Center for Immunology and Infectious Disease, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Eur J Immunol 40:3043-53. 2010
    ....
  14. pmc Regulation of apoptosis through cysteine oxidation: implications for fibrotic lung disease
    Yvonne M W Janssen-Heininger
    Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA
    Ann N Y Acad Sci 1203:23-8. 2010
    ..This manuscript will discuss evidence that S-glutathionylation regulates death receptor induced apoptosis, and the potential implications for cysteine oxidations in the pathogenesis of in fibrotic lung disease...
  15. pmc Reduced myocarditis following Coxsackievirus infection in cellular FLICE inhibitory protein--long form-transgenic mice
    Sally Huber
    Department of Pathology, The University of Vermont College of Medcine, Burlington, VT, USA
    Immunology 119:541-50. 2006
    ..It also produced a Tc2 cytokine profile. These effects of c-FLIP collectively served to diminish the severity of CVB3-induced myocarditis...
  16. ncbi request reprint The death receptor Fas (CD95/APO-1) mediates the deletion of T lymphocytes undergoing homeostatic proliferation
    Karen A Fortner
    Immunobiology Division, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 175:4374-82. 2005
    ..As Fas-deficient lpr mice manifest no significant abnormalities in thymic negative selection or in foreign Ag-induced peripheral T cell deletion, their lymphadenopathy may result from unrestrained homeostatic proliferation...
  17. ncbi request reprint cFLIP regulation of lymphocyte activation and development
    Ralph C Budd
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, Vermont 50405, USA
    Nat Rev Immunol 6:196-204. 2006
    ....
  18. pmc Fas (CD95/APO-1) limits the expansion of T lymphocytes in an environment of limited T-cell antigen receptor/MHC contacts
    Karen A Fortner
    Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Int Immunol 23:75-88. 2011
    ..Thus, Fas shapes the peripheral T-cell repertoire by regulating the survival of a subset of T cells proliferating in response to limited self-peptide/MHC contacts...
  19. ncbi request reprint Effector CD4+ T cells generate intermediate caspase activity and cleavage of caspase-8 substrates
    Ravi S Misra
    University of Vermont, Immunobiology Program, College of Medicine, Burlington, VT 05405, USA
    J Immunol 174:3999-4009. 2005
    ..The current findings define the level of caspase activity and substrates during initiation of T cell cycling...
  20. pmc Oxidative processing of latent Fas in the endoplasmic reticulum controls the strength of apoptosis
    Vikas Anathy
    Department of Pathology, University of Vermont, Burlington, Vermont, USA
    Mol Cell Biol 32:3464-78. 2012
    ..Collectively, these findings illuminate a regulatory switch, a ligand-initiated oxidative processing of latent Fas, that controls the strength of apoptosis...
  21. pmc Redox-based regulation of apoptosis: S-glutathionylation as a regulatory mechanism to control cell death
    Vikas Anathy
    Department of Pathology, University of Vermont College of Medicine, Burlington, 05405, USA
    Antioxid Redox Signal 16:496-505. 2012
    ..Apoptosis can be triggered by a wide variety of stimuli, including death receptor ligands, environmental agents, and cytotoxic drugs. Apoptosis has also been implicated in the etiology of many human diseases...
  22. pmc Proliferating γδ T cells manifest high and spatially confined caspase-3 activity
    Andreas Koenig
    Department of Medicine, Immunobiology Program, The University of Vermont College of Medicine, Burlington, VT 05405, USA
    Immunology 135:276-86. 2012
    ..Hence, the location and amount of active caspases distinguishes effector T-cell subsets and profoundly influences the fate of the T-cell response...
  23. pmc Accumulation of NFAT mediates IL-2 expression in memory, but not naïve, CD4+ T cells
    Oliver Dienz
    Department of Medicine Immunobiology Program, University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405, USA
    Proc Natl Acad Sci U S A 104:7175-80. 2007
    ..Thus, the accumulation of NFATc1 and NFATc2 in memory CD4+ T cells represents a previously uncharacterized regulatory mechanism for the induction of early gene expression after antigen stimulation...
  24. ncbi request reprint Inhibition of apoptosis and caspase-3 in vascular smooth muscle cells by plasminogen activator inhibitor type-1
    Yabing Chen
    Department of Medicine, The University of Vermont, Burlington, Vermont 05405, USA
    J Cell Biochem 92:178-88. 2004
    ..Accordingly, attenuated apoptosis resulting from elevated expression of PAI-1 by VSMC may be attributable, at least in part, to reversible inhibition of caspase-3 by active PAI-1...
  25. pmc Redox amplification of apoptosis by caspase-dependent cleavage of glutaredoxin 1 and S-glutathionylation of Fas
    Vikas Anathy
    Department of Pathology, University of Vermont, Burlington, VT 05405, USA
    J Cell Biol 184:241-52. 2009
    ..As a result, death-inducing signaling complex formation is also increased, and subsequent activation of caspase-8 and -3 is augmented. These results define a novel redox-based mechanism to propagate Fas-dependent apoptosis...
  26. doi request reprint Attenuation of apoptosis and the eye of the beholder
    Burton E Sobel
    Cardiovascular Research Institute, University of Vermont College of Medicine, Burlington, Vermont, USA
    Coron Artery Dis 19:55-8. 2008
    ....
  27. pmc Morphological and cytochemical determination of cell death by apoptosis
    Douglas J Taatjes
    Department of Pathology, University of Vermont, 89 Beaumont Avenue, Burlington, VT, 05405, USA
    Histochem Cell Biol 129:33-43. 2008
    ..This review will highlight many of these methods, and provide a critique on the advantages and disadvantages associated with them for the specific identification of apoptotic cells in culture and tissues...
  28. pmc Interleukin-1 receptor and caspase-1 are required for the Th17 response in nitrogen dioxide-promoted allergic airway disease
    Rebecca A Martin
    Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405, USA
    Am J Respir Cell Mol Biol 48:655-64. 2013
    ..These data implicate a role for caspase-1 and IL-1β in the IL-1 receptor-dependent Th17 response manifest in NO2-promoted allergic airway disease...
  29. ncbi request reprint High expression of Fas ligand by synovial fluid-derived gamma delta T cells in Lyme arthritis
    Karen Roessner
    Department of Medicine Immunobiology, The University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 170:2702-10. 2003
    ..In this capacity, certain gamma delta T cell subsets may serve as cytolytic sentinels at sites of inflammation, and perhaps at epithelial barriers...
  30. ncbi request reprint Cellular FLIP long form-transgenic mice manifest a Th2 cytokine bias and enhanced allergic airway inflammation
    Wenfang Wu
    Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA
    J Immunol 172:4724-32. 2004
    ..Taken together, these results show that c-FLIP(L) can influence cytokine gene expression to promote Th2-driven allergic reaction, in addition to its traditional role of blocking caspase activation induced by death receptors...
  31. pmc The caspase 8 inhibitor c-FLIP(L) modulates T-cell receptor-induced proliferation but not activation-induced cell death of lymphocytes
    Susanne M A Lens
    Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland
    Mol Cell Biol 22:5419-33. 2002
    ..Thus, a major role of c-FLIP(L) in vivo is the modulation of T-cell proliferation by decreasing the T-cell receptor signaling threshold...
  32. pmc Gammadelta T cells promote a Th1 response during coxsackievirus B3 infection in vivo: role of Fas and Fas ligand
    Sally Huber
    Department of Pathology, College of Medicine, The University of Vermont, Burlington, VT 05405, USA
    J Virol 76:6487-94. 2002
    ..These results demonstrate that Fas/FasL interactions conferred by gammadelta T cells on lymphocyte subpopulations may regulate the cytokine response to CVB3 infection and pathogenicity...
  33. ncbi request reprint Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells
    Takao Kataoka
    Department of Bioengineering, Tokyo Institute of Technology, 4259 Nagatsuta cho, Midori ku, Yokohama 226 8501, Japan
    Exp Cell Res 273:256-64. 2002
    ..These findings demonstrate that susceptibility to FasL-induced cell death mainly depends on the expression level of c-FLIP versus cell-surface Fas...
  34. ncbi request reprint The CD95 receptor: apoptosis revisited
    Marcus E Peter
    Ben May Department for Cancer Research, University of Chicago, Chicago, IL 60637, USA
    Cell 129:447-50. 2007
    ..Recent evidence suggests, however, that CD95 mediates not only apoptosis but also diverse nonapoptotic functions depending on the tissue and the conditions...
  35. pmc Apoptosis regulators Fas and Bim cooperate in shutdown of chronic immune responses and prevention of autoimmunity
    Peter D Hughes
    Molecular Genetics of Cancer, The Walter and Eliza Hall Institute of Medical Research, Melbourne 3050, Australia
    Immunity 28:197-205. 2008
    ..These results identify critical overlapping roles for Fas and Bim in T cell death in immune response shutdown and prevention of immunopathology and thereby resolve a long-standing controversy...