U.S. Department of Health and Human Services
Barbara Rehermann
 

 Contact Info

 
Tel: 301-402-7144
Email: barbarar@intra.niddk.nih.gov
 

 Select Experience

 
  • Chief and Senior InvestigatorImmunology Section, Liver Diseases Branch, NIDDK, NIH2004-present
  • HabilitationPrivatdozent of Immunology, Medizinische Hochschule1999
  • Head and Tenure-Track InvestigatorImmunology Section, Liver Diseases Branch, NIDDK, NIH1998-2004
  • HabilitationPrivatdozent of Immunology, Medizinische Hochschule, 1999Clinical Fellow and Independently Funded Investigator, Department of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule1998
  • Postdoctoral Research AssociateLaboratory of Dr. Francis V. Chisari, The Scripps Research Institute1993-1995
  • Medical Intern and ResidentDepartment of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule1993
  • M.D.Medizinische Hochschule1991
 

 Related Links

 

Barbara Rehermann, M.D.

Section Chief, Immunology SectionLiver Diseases Branch
Specialties
  • Immunology
  • Microbiome
  • Virology
  • Gastrointestinal Research
  • Gut Research
  • Liver Research
  • Translational Research

​Research Images

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TitleDescriptionImage
Altered natural killer cell function in chronic viral hepatitisActivated natural killer cells display a similar functional phenotype with increased cytotoxicity (increased TRAIL production, conserved cytotoxicity) and decreased cytokine production in chronic hepatitis B virus infection and in hepatitis C virus infection. This phenotype is induced by type I IFN in hepatitis C virus infection and by TGF-b and IL-10 in hepatitis B virus infection. It can be reversed by treatment-induced viral clearance and/or neutralization of the respective cytokines [for a review, see Cell Mol Gastroenterol Hepatol. 2015;1:578-588].Natural killer cells display increased cytotoxicity and decreased cytokine production in chronic viral hepatitis.Enlarge
Conditions for T cell-mediated immune protection upon hepatitis C virus re-infection.(A) Clearance of a primary HCV infection is associated with strong T cell responses. A secondary HCV infection results in lower HCV titers and more rapid viral clearance. An early memory T cell recall response is detectable in both liver and blood. (B) Depletion of CD4 T cells prior to secondary HCV infection results in weak recall responses, incomplete T-cell mediated control of viremia and emergence of MHC class I escape mutations. Chronic infection ensues. (C) T cell responses that are induced by repeated exposure to trace amounts of HCV, in the absence of quantifiable systemic viremia and seroconversion, do not confer immune protection upon HCV re-infection. The absence of immune protection is associated with an expansion of regulary CD4 T cells during subinfectious HCV exposure and subsequent HCV challenge (see Immunity 2014;40:13-24 and Nature Medicine, 2013:19:1638-1642)Low level HCV exposures abrogate protection from HCV reinfection due to induction of regulatory CD4 T cells.Enlarge
Hepatitis C virus induces and evades innate immune responses in the liver.(A) Hepatitis C virus (HCV)-infected hepatocytes form clusters (indicated in green) in the infected liver. (B) In infected hepatoctyes, HCV is recognized by intracellular pattern recognition receptors, which would normally induce interferon beta and proinflammatory cytokines. However, the HCV protein NS3-4A cleaves both the adapter molecules MAVS and TRIF downstream of the intracellular pattern recognition receptors and thereby blocks the induction of cytokines in infected cells. (c) HCV persists despite increased expression of interferon-stimulated genes in the liver. IFN-b production is abrogated in the upper right hepatocytes due to intracellular expression of HCV NS3-4A. Nonparenchymal cells, e.g. Kupffer cells, plasmacytoid DCs and myeloid DCs contribute to the production of IFNs that induce interferon-stimulated genes in HCV-uninfected hepatocytes [see Immunity 2014;40:13-24].Hepatitis C virus induces and evades innate immune responses in the liver.Enlarge
Wild Mouse Gut Microbiota Promotes Host Fitness and Improves Disease ResistanceScientists from the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases led research finding that transferring the gut microbes from wild mice to laboratory mice promoted fitness and significantly improved responses to an otherwise lethal flu virus infection and to colorectal cancer. By making lab mice more closely mirror real-world mice, the approach may improve the odds of success as research moves from mouse to man. The method could also help advance studies in metabolism, behavior, and endocrinology. The results published in Cell: www.cell.com/cell/fulltext/S0092-8674(17)31065-6
Gut microbes from wild mice protect lab mice against lethal influenza infection and colitis-associated tumorigenesis.The image details the generation of a mouse model that combines the tractable genetics of standard laboratory mice and the fitness promoting traits of wild mouse gut microbiota. Characterization of the wild mouse microbiome opens a window of opportunity to understand how the gut microbiota affects aspects of host physiology that are important in the natural world outside the laboratory [from: Cell, 171: 1015-1028, 2017]Gut microbes from wild mice protect lab mice against lethal influenza infection and colitis-associated tumorigenesis.Enlarge