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Elizabeth Blankenhorn

Elizabeth Blankenhorn, PhD

Professor


Department: Microbiology & Immunology

Education

  • PhD - California Institute of Technology (1979)

Dr. Blankenhorn is a professor in the Department of Microbiology & Immunology at Drexel University College of Medicine.

Research Overview

Research interests: Genetic foundations for inherited susceptibility to autoimmune diseases, including diabetes, scleroderma and multiple sclerosis. Impact of genetics on wound healing and susceptibility to viral infection.

Research staff: Laura Cort and Alan Bocage

Graduate students: Ryan Eberwine, Chelsea Burgwin, Frank Bearoff

Research Interests

Genetic foundations for inherited susceptibility to autoimmune diseases, including diabetes, scleroderma and multiple sclerosis. Impact of genetics on wound healing and susceptibility to viral infection.

Research

ANA antibodies from a scleroderma mouse model.

ANA antibodies from a scleroderma mouse model.

The goal of the research in our laboratory is to understand the genetic basis for inherited susceptibility to viral infections and to autoimmune diseases, including diabetes, scleroderma, and multiple sclerosis. We also have a long-standing interest in the genetic architecture of wound healing. In our work, backcross and F2 progeny are screened for alleles at a large number of genetic loci. The inheritance of these alleles is compared to the inheritance of the phenotype (“linked”) and a preliminary assignment of the location of incidence and quantitative trait loci (QTL) is made. The QTL are confirmed in subsequent crosses, or are fixed in the genome by selective breeding, for the purpose of positional cloning and identification of the disease gene itself.

Skin from a scleroderma mouse model and control.

Skin from a scleroderma mouse model and control.

We currently have several projects underway, including studies to examine the genetic control and the sexual dimorphism of susceptibility to mouse experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis. A second project is to map autoimmune diabetes-susceptibility loci in the LEW.1WR1 rat, the prototype strain for this phenotype, and to understand the role of the TCR haplotype in this disease. We are extending our finding that diabetes in both LEW.1WR1 and DP-BB rats is controlled by a QTL we discovered on chromosome 4.  We now are in the process of identifying a second QTL on chromosome 20, which may well be homologous to one or more loci in human Type 1 diabetes. Our lab has a third study underway to identify the genetic basis of the Tsk2/+ (tight skin) mutation. A fourth major study concerns the role of the innate immune system in the control of HSV-induced encephalitis in young mice.  Finally, in collaboration with the Wistar Institute, we are mapping wound healing genes in several large crosses to confirm our original mapping of six QTL associated with the trait of wound healing/regeneration, and to understand the significant sexual dimorphism in the genetic control of this trait.

Mapping a diabetes gene in rats and human cohorts: Ubd is a candidate gene
Mapping a diabetes gene in rats and human cohorts: Ubd is a candidate gene.

Publications

Selected Publications
(See all Elizabeth Blankenhorn's publications in PubMed.)

"Prevention of type 1 diabetes in the rat with an allele-specific anti-T-cell receptor antibody: Vβ13 as a therapeutic target and biomarker"
Liu Z, Cort L, Eberwine R, Herrmann T, Leif JH, Greiner DL, Yahalom B, Blankenhorn, EP, and JP Mordes
Diabetes, 61(5): 1160-1168, 2012.

"Genetics of EAE Supports the Role of T Helper Cells in MS Pathogenesis"
Blankenhorn EP, Butterfield R, Case LK, Wall EH, del Rio R, Diehl SA, Krementsov D, Saligrama N, and C Teuscher
Ann. Neurol., 70(6): 887-896, 2011.

"Multiple linked quantitative trait loci within the Tmevd2/Eae3 interval control the severity of experimental allergic encephalomyelitis in DBA/2J mice"
Spach KM, Case LK, Noubade R, Petersen CB, McElvany B, Zalik N, Hickey WF, Blankenhorn EP, and C Teuscher
Genes and Immunity, 11(8): 649-659, 2010.

The postnatal maternal environment affects autoimmune disease susceptibility in A/J mice.
Case LK, Del Rio R, Bonney EA, Zachary JF, Blankenhorn EP, Tung KS, and C Teuscher.
Immunology & Cell Biology 260(2): 119-127, 2010.

Infection with viruses from several families triggers autoimmune diabetes in LEW.1WR1 rats: prevention of diabetes by maternal immunization. ?
Tirabassi RS, Guberski DL, Blankenhorn EP, Leif JH, Woda BA, Liu Z, Winans D, Greiner DL, and JP Mordes
Diabetes, 59(1): 110-118, 2009.

A single nucleotide polymorphism in Tyk2 controls susceptibility to experimental allergic encephalomyelitis. 
Spach KM, Noubade R, McElvany B, Hickey WF, Blankenhorn EP, and C Teuscher.
The Journal of Immunology, 182(12): 7776-7783, 2009.

Cutting edge: the Y chromosome controls the age-dependent experimental allergic encephalomyelitis sexual dimorphism in SJL/J mice.
 ?Spach KM, Blake M, Bunn JY, McElvany B, Noubade R, Blankenhorn EP, an C Teuscher.
The Journal of Immunology, 182: 1789-1793, 2009.

Analysis of the rat Iddm14 diabetes susceptibility locus in multiple rat strains: identification of a susceptibility haplotype in the Tcrb-V  locus.?
Mordes JP, Cort L, Norowski E, Leif J, Fuller JM, Lernmark A, Greiner DL, and EP Blankenhorn.?
Mammalian Genome, 2009 (3): 162-169, 2009.

Virus-induced autoimmune diabetes in the LEW.1WR1 rat requires Iddm14 and a locus proximal to the major histocompatibility complex.
Blankenhorn EP, Cort L, Greiner DL, Guberski DL, and JP Mordes.
Diabetes, 58: 2930-2938, 2009.

Genetic loci that regulate healing and regeneration in LG/J and SM/J mice.
Blankenhorn EP, Bryan G, Kossenkov AV, Clark LD, Zhang XM, Chang C, Horng W, Pletscher LS, Cheverud JM, Showe LC, and E Heber-Katz?Mamm.
Genome, 20: 720-733. 2009.

Central histamine H3 receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS.
Teuscher C, Subramanian M, Noubade R, Gao JF, Offner H, Zachary JF, and EP Blankenhorn.
Proceedings of the National Academy of Sciences of the United States of America, 104(24): 10146-10151, 2007.

Histamine receptor H1 is required for TCR-mediated p38 MAPK activation and optimal IFN-gamma production in mice.
Noubade R, Milligan G, Zachary JF, Blankenhorn EP, del Rio R, Rincon M, and C Teuscher.?
Journal of Clinical Investigation 117(11): 3507-3518, 2007.

Evidence that the Y-Chromosome influences EAE in male and female mice.
Teuscher C, Noubade R, Spach K, Bunn JY, Fillmore PD, Zachary JF, and EP Blankenhorn
Proceedings of the National Academy of Sciences. 103: 8024-8029, 2006.

et al.  Complex Trait Consortium.  The nature and identification of quantitative trait loci: a community's view.?
Abiola O, Angel JM, Avner P, Bachmanov AA, Belknap JK, Bennett B, Blankenhorn EP
Nature Reviews Genetics, 4: 911-916, 2003.

Identification of Bphs, an Autoimmune Disease Locus, as Histamine Receptor H1.?
Ma RZ, Gao J, Meeker ND, Fillmore PD, Tung KSK, WatanabeT, Zachary JF, Offner H, Blankenhorn EP, and C Teuscher.?
Science, 297: 620-623,  2002


Contact Information


Research Office

Department of Microbiology & Immunology
2900 W. Queen Lane
Philadelphia, PA 19129
Phone: 215.991.8392
Fax: 215.848.2271