|
 Robinna
G. Lorenz, PhD
Associate Professor
of Pathology
1530
Third Avenue South--BBRB 730 (zip 35294-2170)
Phone:
: (205) 934-0676 or (205) 934-6794 Email:
rlorenz@uab.edu
Affiliations
Department of Pathology
Division of Laboratory
Medicine
Department of Microbiology
Biographical
Sketch (Community
of Science - Profile)
Robin Lorenz received her M.D.,
Ph.D. in Immunology from Washington University in St. Louis in 1990. She then
completed her residency in Clinical Pathology at Barnes-Jewish Hospital, while
also doing postdoctoral research in Gastrointestinal Biology at Washington
University in St. Louis. Dr. Lorenz was hired at Washington University as an
Assistant Professor of Pathology and Medicine in 1994. In addition, she served
as the Medical Director of the Joint Clinical Immunology Laboratory for
Barnes-Jewish and St. Louis Children’s Hospitals and as the Associate Director
of the Laboratory Medicine Residency Training Program. Dr. Lorenz joined the UAB
faculty in 2002 as an Associate Professor in the Department of Pathology. The
National Institutes of Health and the American Cancer Society fund her
laboratory research investigating the mucosal immune system. She is married and
has two children.
Research
(Interests: Inflammation,
Mucosal Immunology
)
The focus
of research in Dr. Lorenz's laboratory is the study of the cellular components
of the mucosal immune system and their interactions with the gastrointestinal
epithelium and luminal contents. The host response to luminal antigens includes
mucosal immunity, oral tolerance, uncontrolled infection, or autoimmunity. The
first area of interest is the cellular immune response to Helicobacter in a
mouse model of gastric infection and inflammation. The bacteria Helicobacter
pylori is a major pathogen which is linked to acute and chronic gastritis,
gastric and duodenal ulcer disease, mucosal-associated lymphomas, and
adenocarcinoma. Gastric cancer is the second most common cause of cancer
mortality in the world. Infection with H. pylori results in an early gastric
infiltration of neutrophils, natural killer cells, CD4+ T-cells, and plasma
cells. These gastric infiltrates lead to alterations in gastric epithelial cell
differentiation, function, and turnover. The critical factors which lead to
these changes are unknown, but it is clear that this gastric epithelial cell
dysplasia leads to an increased risk of gastric cancer. Through the use of a
murine model of Helicobacter infection which closely mimics the human disease,
we have done a careful analysis of the host immune response to Helicobacter
infection. Using a novel adoptive transfer model of disease, the group has shown
that it is the host CD4+ T-cell response, which is crucial for the development
of H. felis associated gastric dysplasia. They have further demonstrated
that this dysplasia subsequently develops into gastric adenocarcinoma. In mice
infected for > 1 year, 58% (14/24) developed foci of gastric adenocarcinoma. Dr.
Lorenz is currently focused on dissecting out which components of the
inflammation are critical in the progression from dysplasia to adenocarcinoma.
In addition, the laboratory is studying a novel mouse model of low grade
MALT-lymphoma induced by Helicobacter-infection. The second area of focus in the
laboratory is the role of the intestinal epithelium and innate immune responses
in the development of inflammatory bowel disease. They are investigating these
interactions in a spontaneous model of colonic inflammation that occurs in the
absence of the multidrug resistance protein 1a.
Publications (open
Pubmed
in new window)
(Updated January, 2006) |
