Rodney D. Newberry, M.D.

Washington University
School of Medicine

Dept. of Medicine
Div. of Gastroenterology
Box 8124
660 S. Euclid Ave.
St. Louis, MO 63110

tel: (314) 362-5291
fax: (314) 747-2048
email: rnewberry@wustl.edu
web: Personal Weblink

 

 

RESEARCH INTEREST

My research interests center on understanding the mechanisms for controlling the organization and function of lymphocytes within the intestine. The gastrointestinal immune system is continuously exposed to luminal antigens in the form of normal microbial flora and non-pathogenic dietary antigens. Crucial to normal gastrointestinal function is the ability of the gastrointestinal immune system to avoid a potentially damaging inflammatory response to non-pathogenic luminal antigens, despite the concurrent exposure to bacterial stimuli known to induce inflammatory responses in more traditional lymphoid organs. The mucosal immune system utilizes multiple approaches to prevent inappropriate inflammatory responses in the intestine. These include the production of secretory IgA directed against commensal and pathogenic bacteria and the production of immunomodulatory cytokines by T-lymphocytes in the intestinal lamina propria. Recruiting and organizing lymphocyte populations appropriately is critical for these functions.

The lymphotoxin beta receptor (LTβR) is a tumor necrosis factor receptor superfamily member with an established role in the formation and organization of secondary lymphoid structures. We have identified a novel roles for the LTβR in directing the entry and residence of B-2 B-lymphocytes within the intestinal lamina propria, and in directing the formation of tertiary lymphoid structures in the small intestine, or isolated lymphoid follicles (ILFs). The function of tertiary lymphoid structures is unclear, but it has been suggested that these structures may contribute to inappropriate inflammatory responses by allowing uncontrolled interactions between lymphocytes, antigens, and antigen presenting cells. My laboratory is currently engaged in studies to identify the stimuli and downstream factors inducing ILF formation in the intestine, and to understand the function of ILFs in health and disease.

SELECTED PUBLICATIONS

Newberry RD, and Lorenz RG: Isolated Lymphoid Follicle Formation. Proceedings of the New York Academy of Sciences pending publication 2004.

Gurtner GJ, Newberry RD, Schloemann S, McDonald KG, and Stenson WF, Inhibition of Indoleamine 2,3-Dioxygenase Augments Trinitrobenzene Sulfonic Acid Colitis in Mice, Gastroenterology,2003;125:1762-1773.

Lorenz RG, Chaplin DD, McDonald KG, McDonough JS, Newberry RD. Isolated lymphoid follicle formation is inducible and dependent upon lymphotoxin-sufficient B lymphocytes, lymphotoxin beta receptor, and TNF receptor I function. Journal of Immunology. 2003;170:5475-82.

Newberry RD, McDonough JS, McDonald KG, Lorenz RG. Postgestational lymphotoxin/lymphotoxin beta receptor interactions are essential for the presence of intestinal B lymphocytes. Joournal of Immunology. 2002;168:4988-97.

Newberry RD, McDonough JS, Stenson WF, Lorenz RG. Spontaneous and continuous cyclooxygenase-2-dependent prostaglandin E2 production by stromal cells in the murine small intestine lamina propria: directing the tone of the intestinal immune response. Journal of Immunology. 2001;166:4465-72.

Newberry RD, Stenson WF, Lorenz RG: Cyclooxygenase-2-dependent arachidonic acid metabolites are essential modulators of the intestinal immune response to dietary antigen. Nature Medicine, 1999; 5 (8) 900-6,