William O'Connor Jr, PhD
Areas of Study
- Yale University2011Postdoctoral
- University of North Carolina at Chapel Hill2004PhD
In the gastrointestinal tract, immune sensing of luminal content influences resident microbial communities, and the microbiota in turn educate cells of the immune system. These events drive powerful immune and inflammatory processes locally and in distal organ systems. The level of coordination and extent of signal integration in determining inflammatory outcomes in the GI is remarkable. Signals derived from resident and infiltrating immune cells, stromal cells, and the commensal microbiota all contribute, and most of this signal integration remains poorly understood.
Our long-term goal is to understand how inflammation and mucosal healing are controlled. Improper immunoregulation at the mucosa is thought to drive a number of inflammatory disorders, including the inflammatory bowel diseases (IBDs), and may facilitate the progression to neoplasia.
Among the myriad of soluble factors controlling the initiating and resolving phases of inflammatory processes are cytokines, which participate in both pro-inflammatory signaling as well as in mucosal healing. Cytokines are generally pleotrophic and function in a microenvironment- and context-specific fashion. In the intestine, cytokines may be pro-inflammatory, anti-inflammatory, or 'inflammation-neutral'. Th17-associated cytokines are of particular interest, modulating immune cell recruitment, antimicrobial host defense, and tissue-protective processes. Cytokine function and integrated responses are a recurring theme in our research and are long-standing interests. We are currently investigating several novel mechanisms governing inflammation and mucosal healing in the GI tract.
Cell-surface perturbations of the epidermal growth factor and vascular endothelial growth factor receptors by phosphorothioate oligodeoxynucleotides. Rockwell P, O'Connor WJ, King K, Goldstein NI, Zhang LM, Stein CA. Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6523-8.
Antivascular endothelial growth factor receptor (fetal liver kinase 1) monoclonal antibody inhibits tumor angiogenesis and growth of several mouse and human tumors. Prewett M, Huber J, Li Y, Santiago A, O'Connor W, King K, Overholser J, Hooper A, Pytowski B, Witte L, Bohlen P, Hicklin DJ. Cancer Res. 1999 Oct 15;59(20):5209-18.
Monoclonal antibody to vascular endothelial-cadherin is a potent inhibitor of angiogenesis, tumor growth, and metastasis. Liao F, Li Y, O'Connor W, Zanetta L, Bassi R, Santiago A, Overholser J, Hooper A, Mignatti P, Dejana E, Hicklin DJ, Bohlen P. Cancer Res. 2000 Dec 15;60(24):6805-10.
Mechanisms of nuclear import and export that control the subcellular localization of class II transactivator. J. Immunol. 2001 Oct 1;167(7):3626-34. Cressman DE, O'Connor WJ, Greer SF, Zhu XS, Ting JP.
View William O'Connor Jr.'s articles on the National Institute of Health's PubMed website.