Laura Pope Hale

Professor of Pathology

CMB - Clinical/Other

Campus mail: 207A Davison Bldg, Durham, NC 27710

Phone: (919) 684-4771

The Hale laboratory employs techniques of cellular and molecular biology to study mechanisms responsible for the generation of both normal immune responses and immune-mediated diseases. Research in the laboratory is mainly focused on inflammatory bowel disease (IBD), an immune-mediated disorder that is hypothesized to result from the abnormal immune response of a genetically susceptible host to the antigens derived from enteric bacteria. Development of optimal treatments for disease requires a detailed understanding of mechanisms of disease pathogenesis. Thus current work in the laboratory is aimed at understanding triggers of intestinal inflammation and mechanisms of inflammation-associated neoplasia, in addition to developing novel therapies for IBD treatment. Ongoing research also includes investigating mechanisms that determine the immunogenicity of oral antigens, to develop novel adjuvants for oral vaccines. This work has relevance for pathogenesis and treatment of infectious diseases affecting the gastrointestinal tract, as well as for inflammatory bowel disease.

Dr. Hale is an expert in pathologic evaluation of colitis and immunodeficiency in both humans and mice and is board-certified in Anatomic and Clinical Pathology.

Education and Training

Michigan State University, B.S. 1980
Rutgers University, M.S. 1984
Duke University, Ph.D. 1990
Duke University, M.D. 1991
Duke University, Resident, Anatomic & Clinical Pathology, Pathology

Selected Grants and Awards

Publications

2C9 anti-BRCA2

A genetically modified allogeneic cellular vaccine generates MHC class I-restricted cytotoxic responses against tumor-associated antigens and protects against CNS tumors in vivo.

An active immunotherapeutic strategy using transfected allogeneic cells for targeting the mutant epidermal growth factor receptor (EGFRvIII) on intracranial tumors was examined.

A mouse model for hereditary hemorrhagic telangiectasia (HHT) type 2.

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal-dominant disorder characterized by the age-dependent development of focal arteriovenous malformations and telangiectases.

A murine model for hereditary hemorrhagic telangiectasia type 2.

A novel murine model of inflammatory bowel disease and inflammation-associated colon cancer with ulcerative colitis-like features.

Mutations that increase susceptibility to inflammatory bowel disease (IBD) have been identified in a number of genes in both humans and mice, but the factors that govern how these mutations contribute to IBD pathogenesis and result in phenotypic p

Abnormal development of thymic dendritic and epithelial cells in human X-linked severe combined immunodeficiency.

The X-linked form of severe combined immunodeficiency (X-SCID) is caused by mutations in the common cytokine receptor gamma chain and results in lack of T and NK cells and defective B cells.