Physician
Anesthesiology
Dr. Stephen H. Gregory, MD
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Stephen Gregory works in the field of Anesthesiology. He researched medicine at Saint Louis University School of Medicine. Saint Louis University School of Medicine has a rank of 67 in research and a 57 in primary care Stephen H. Gregory, MD is also published. He has 52 publications published. The lastest publication: "Neutrophil-Kupffer-cell interaction in host defenses to systemic infections.'
Publications
- Aspartate-β-hydroxylase induces epitope-specific T cell responses in hepatocellular carcinoma.
- HCV Epitope, Homologous to Multiple Human Protein Sequences, Induces a Regulatory T Cell Response in Infected Patients.
- Increasing Hepatitis C Prevalence and Associated Risk Behaviors among Incarcerated Young Adults.
- Peptide-pulsed dendritic cells induce the hepatitis C viral epitope-specific responses of naïve human T cells.
- Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function.
- Improved antimicrobial host defense in mice following poly-(1,6)-β-D-glucopyranosyl-(1,3)-β-D-glucopyranose glucan treatment by a gender-dependent immune mechanism.
- Targeting the diverse immunological functions expressed by hepatic NKT cells.
- NK cells suppress experimental cholestatic liver injury by an interleukin-6-mediated, Kupffer cell-dependent mechanism.
- Detoxified endotoxin vaccine (J5dLPS/OMP) protects mice against lethal respiratory challenge with Francisella tularensis SchuS4.
- Neutrophil depletion blocks early collagen degradation in repairing cholestatic rat livers.
- Neutrophils sequestered in the liver suppress the proinflammatory response of Kupffer cells to systemic bacterial infection.
- Epitope-based vaccination against pneumonic tularemia.
- Laser capture microdissection and genetic analysis of carbon-labeled Kupffer cells.
- Invariant natural killer T cells suppress the neutrophil inflammatory response in a mouse model of cholestatic liver damage.
- The role of hepatic invariant NKT cells in systemic/local inflammation and mortality during polymicrobial septic shock.
- Generation of immune responses against hepatitis C virus by dendritic cells containing NS5 protein-coated microparticles.
- Hepatic macrophages promote the neutrophil-dependent resolution of fibrosis in repairing cholestatic rat livers.
- Generation and characterization of an immunogenic dendritic cell population.
- Tularemia vaccines - an overview.
- CD8+ T cells promote inflammation and apoptosis in the liver after sepsis: role of Fas-FasL.
- Diversity of Francisella tularensis Schu4 antigens recognized by T lymphocytes after natural infections in humans: identification of candidate epitopes for inclusion i...
- Kupffer cells abrogate cholestatic liver injury in mice.
- Vaccination with protein-transduced dendritic cells elicits a sustained response to hepatitis C viral antigens.
- Role of alveolar macrophage and migrating neutrophils in hemorrhage-induced priming for ALI subsequent to septic challenge.
- Repair after cholestatic liver injury correlates with neutrophil infiltration and matrix metalloproteinase 8 activity.
- Type 1 interferon augments DNA-based vaccination against hepatitis C virus core protein.
- Host resistance of CD18 knockout mice against systemic infection with Listeria monocytogenes.
- Differential effects of macrophage inflammatory chemokine-2 and keratinocyte-derived chemokine on hemorrhage-induced neutrophil priming for lung inflammation: assessme...
- Shock-induced neutrophil mediated priming for acute lung injury in mice: divergent effects of TLR-4 and TLR-4/FasL deficiency.
- Neutrophil-Kupffer cell interaction: a critical component of host defenses to systemic bacterial infections.
- Listeria monocytogenes: clinical and experimental update.
- Complementary adhesion molecules promote neutrophil-Kupffer cell interaction and the elimination of bacteria taken up by the liver.
- Flt3 ligand pretreatment promotes protective immunity to Listeria monocytogenes.
- An updated model of cell-mediated immunity--listeriosis: clinical and research aspects.
- From hot dogs to CD8+ T cells: Listeria monocytogenes.
- CD8+ T-cell-mediated response to Listeria monocytogenes taken up in the liver and replicating within hepatocytes.
- Neutrophil-Kupffer-cell interaction in host defenses to systemic infections.
- Fas (CD95)-dependent cell-mediated immunity to Listeria monocytogenes.
- IL-6 produced by Kupffer cells induces STAT protein activation in hepatocytes early during the course of systemic listerial infections.
- Listeria monocytogenes-infected hepatocytes are targets of major histocompatibility complex class Ib-restricted antilisterial cytotoxic T lymphocytes.
- Internalin B promotes the replication of Listeria monocytogenes in mouse hepatocytes.
- Immune CD8+ T lymphocytes lyse Listeria monocytogenes-infected hepatocytes by a classical MHC class I-restricted mechanism.
- Lymphokine-activated killer cells lyse Listeria-infected hepatocytes and produce elevated quantities of interferon-gamma.
- Expression of the inlAB operon by Listeria monocytogenes is not required for entry into hepatic cells in vivo.
- Bacteria in the bloodstream are trapped in the liver and killed by immigrating neutrophils.
- Hepatocytes can serve as accessory cells in the response of immune T lymphocytes to heat-killed Listeria monocytogenes.
- Arginine analogues suppress antigen-specific and -nonspecific T lymphocyte proliferation.
- Rapamycin but not FK506 inhibits the proliferation of mononuclear phagocytes induced by colony-stimulating factors.
- Evaluation of the influence of FK 506, rapamycin, and cyclosporine on processing and presentation of particulate antigen by macrophages: assessment of a drug "carry-ov...
- The role of colony-stimulating factors in host defenses.
- Accessory function of Kupffer cells in the antigen-specific blastogenic response of an L3T4+ T-lymphocyte clone to Listeria monocytogenes.
Schools
Saint Louis University School of Medicine
Doctors Specialties
- Anesthesiology
Accepted Insurances
- Medicaid
- Medicare MCR
Education
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Duke University Hospital -
Saint Louis University School of Medicine
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