Kathleen M Gilbert

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. ncbi Epigenetic alterations may regulate temporary reversal of CD4(+) T cell activation caused by trichloroethylene exposure
    Kathleen M Gilbert
    Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
    Toxicol Sci 127:169-78. 2012
  2. ncbi T cell tolerance induced by histone deacetylase inhibitor is mediated by P21cip1
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock 72205, USA
    Immunopharmacol Immunotoxicol 27:545-64. 2005
  3. ncbi Butyric acid derivative induces allospecific T cell anergy and prevents graft-versus-host disease
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Immunopharmacol Immunotoxicol 25:13-27. 2003
  4. ncbi Environmental contaminant and disinfection by-product trichloroacetaldehyde stimulates T cells in vitro
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72205, USA
    Int Immunopharmacol 4:25-36. 2004
  5. ncbi Delineating liver events in trichloroethylene-induced autoimmune hepatitis
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Chem Res Toxicol 22:626-32. 2009
  6. ncbi Structure-activity relationship between carboxylic acids and T cell cycle blockade
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, 72202, USA
    Life Sci 78:2159-65. 2006
  7. ncbi Coexposure to mercury increases immunotoxicity of trichloroethylene
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, College of Medicine, Arkansas, USA
    Toxicol Sci 119:281-92. 2011
  8. ncbi Chronic exposure to a trichloroethylene metabolite in autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia
    Sarah J Blossom
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Toxicol Sci 95:401-11. 2007
  9. ncbi Histone deacetylase inhibitors induce antigen specific anergy in lymphocytes: a comparative study
    R Erik Edens
    Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR, USA
    Int Immunopharmacol 6:1673-81. 2006
  10. ncbi Macrophage production of inflammatory mediators is potently inhibited by a butyric acid derivative demonstrated to inactivate antigen-stimulated T cells
    Lee S F Soderberg
    Department of Microbiology and Immunology, College of Medicine, University of Arkansas for Medical Sciences, 4301 W Markham Steet, Little Rock, AR 72205, USA
    Int Immunopharmacol 4:1231-9. 2004

Research Grants

  1. Determining how trichloroethylene alters CD4+ T cell function
    Kathleen M Gilbert; Fiscal Year: 2010
  2. Determining how trichloroethylene alters CD4+ T cell function
    Kathleen M Gilbert; Fiscal Year: 2011

Collaborators

Detail Information

Publications16

  1. ncbi Epigenetic alterations may regulate temporary reversal of CD4(+) T cell activation caused by trichloroethylene exposure
    Kathleen M Gilbert
    Arkansas Children s Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72202, USA
    Toxicol Sci 127:169-78. 2012
    ..Thus, these results described the biphasic nature of TCE-induced alterations in CD4(+) T cell function and suggested that these changes represented potentially reversible alterations in epigenetic processes...
  2. ncbi T cell tolerance induced by histone deacetylase inhibitor is mediated by P21cip1
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock 72205, USA
    Immunopharmacol Immunotoxicol 27:545-64. 2005
    ..These results underscore the role of p21cip1 in mediating T cell tolerance induced by the histone deacetylase inhibitor MEB...
  3. ncbi Butyric acid derivative induces allospecific T cell anergy and prevents graft-versus-host disease
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Immunopharmacol Immunotoxicol 25:13-27. 2003
    ..The use of MEB to inactivate host-specific T cells ex vivo underlines the potential clinical importance of this compound in the prevention and treatment of unwanted immune responses such as GVHD...
  4. ncbi Environmental contaminant and disinfection by-product trichloroacetaldehyde stimulates T cells in vitro
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72205, USA
    Int Immunopharmacol 4:25-36. 2004
    ..By demonstrating that TCAA can stimulate T-cell function directly, these results may explain how the environmental toxicant trichloroethylene promotes T-cell activation and related autoimmunity in vivo...
  5. ncbi Delineating liver events in trichloroethylene-induced autoimmune hepatitis
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Chem Res Toxicol 22:626-32. 2009
    ....
  6. ncbi Structure-activity relationship between carboxylic acids and T cell cycle blockade
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, 72202, USA
    Life Sci 78:2159-65. 2006
    ..These results underline the relationship between the ability of a carboxylic acid to inhibit histone deacetylation, and their ability to block T cell proliferation, and suggests that branching inhibits these effects...
  7. ncbi Coexposure to mercury increases immunotoxicity of trichloroethylene
    Kathleen M Gilbert
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, College of Medicine, Arkansas, USA
    Toxicol Sci 119:281-92. 2011
    ..Coexposure to TCE and HgCl(2) also generated a unique liver-specific antibody response not found in mice exposed to a single toxicant. This finding stresses the importance of including mixtures in assessments of chemical immunotoxicity...
  8. ncbi Chronic exposure to a trichloroethylene metabolite in autoimmune-prone MRL+/+ mice promotes immune modulation and alopecia
    Sarah J Blossom
    Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences Arkansas Children s Hospital Research Institute, Little Rock, Arkansas 72202, USA
    Toxicol Sci 95:401-11. 2007
    ..Taken together, a chronic exposure to TCAH promotes alopecia and skin inflammation. The early effects of TCAH on MMP-7 levels may provide a mechanism by which TCAH promotes skin pathology...
  9. ncbi Histone deacetylase inhibitors induce antigen specific anergy in lymphocytes: a comparative study
    R Erik Edens
    Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR, USA
    Int Immunopharmacol 6:1673-81. 2006
    ..These results will guide future studies examining HDAIs for ability to induce clinical tolerance in organ transplantation...
  10. ncbi Macrophage production of inflammatory mediators is potently inhibited by a butyric acid derivative demonstrated to inactivate antigen-stimulated T cells
    Lee S F Soderberg
    Department of Microbiology and Immunology, College of Medicine, University of Arkansas for Medical Sciences, 4301 W Markham Steet, Little Rock, AR 72205, USA
    Int Immunopharmacol 4:1231-9. 2004
    ..Thus, while inducing specific T cell unresponsiveness, MEB also exerts anti-inflammatory activity by acting on macrophages to suppress production of cytokines and NO...
  11. ncbi Exposure to a metabolite of the environmental toxicant, trichloroethylene, attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Toxicol Sci 92:103-14. 2006
    ..This represents a mechanism by which an environmental trigger inhibits AICD in CD4+ T cells and may thereby promote CD4+ T cell-mediated autoimmune disease...
  12. ncbi Histone deacetylase inhibitor uses p21(Cip1) to maintain anergy in CD4+ T cells
    A Selma Dagtas
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, USA
    Int Immunopharmacol 9:1289-97. 2009
    ..Thus, p21(Cip1) appears to mediate the proliferative unresponsiveness found in CD4+ T cell anergized by exposure to Ag in the presence of HDAC inhibitors...
  13. ncbi p21(Cip1) up-regulated during histone deacetylase inhibitor-induced CD4(+) T-cell anergy selectively associates with mitogen-activated protein kinases
    Ayse Selma Dagtas
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, Little Rock, AR 72202, USA
    Immunology 129:589-99. 2010
    ..The n-butyrate-induced p21(Cip1)-mediated inhibition of JNK and c-jun represents a novel potential mechanism by which proliferative unresponsiveness was maintained in CD4(+) T cells...
  14. ncbi The ability of antigen, but not interleukin-2, to promote n-butyrate-induced T helper 1 cell anergy is associated with increased expression and altered association patterns of cyclin-dependent kinase inhibitors
    Stephanie K Jackson
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Immunology 106:486-95. 2002
    ..In addition, p21Cip1 may inhibit proliferation in the anergic Th1 cells by some mechanism other than suppression of cdks that is unique to the induction of Th1 cell anergy...
  15. ncbi Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid
    Sarah J Blossom
    Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children s Hospital Research Institute, 1120 Marshall Street, Little Rock, AR 72205, USA
    J Autoimmun 23:211-20. 2004
    ..By demonstrating that TCAH and TCA can activate CD4+ T cells and inhibit their apoptosis following in vivo exposure represents a mechanism by which environmental toxicants may induce or accelerate the development of autoimmune disease...
  16. ncbi Postnatal exposure to trichloroethylene alters glutathione redox homeostasis, methylation potential, and neurotrophin expression in the mouse hippocampus
    Sarah J Blossom
    Department of Pediatrics, University of Arkansas for Medical Sciences, College of Medicine, Arkansas Children s Hospital Research Institute, 13 Children s Way, Little Rock, AR 72202, United States Electronic address
    Neurotoxicology 33:1518-27. 2012
    ..Our results demonstrate that low-level postnatal and early life TCE exposure modulates neurotrophin gene expression in the mouse hippocampus and may provide a mechanism for TCE-mediated neurotoxicity...

Research Grants2

  1. Determining how trichloroethylene alters CD4+ T cell function
    Kathleen M Gilbert; Fiscal Year: 2010
    ..Consequently, demonstrating that a common water pollutant such as trichloroethylene can cause this effect and describing the mechanism for it could have important implications for human health. ..
  2. Determining how trichloroethylene alters CD4+ T cell function
    Kathleen M Gilbert; Fiscal Year: 2011
    ..Consequently, demonstrating that a common water pollutant such as trichloroethylene can cause this effect and describing the mechanism for it could have important implications for human health. ..