Andrea J. Tenner
Molecular Biology & Biochemistry, School of Biological Sciences
Pathology, School of Medicine
Neurobiology and Behavior, School of Biological Sciences
Phone: (949) 824-3268
Email: atenner@uci.edu
darwin.bio.uci.edu/~faculty/tenner/
http://www.faculty.uci.edu/scripts/UCIFacultyProfiles/detailMBB.cfm?ID=2679
http://www.faculty.uci.edu/profile.cfm?faculty_id=2679
Andrea Tenner
A unifying goal of Dr. Tenner’s research program is to identify targets and/or pathways within the innate immune system to inhibit detrimental inflammation (via inhibition of complement activation or inflammatory effector mechanisms induced by complement activation) and enhance the antiinflammatory, reparative or protective processes in response to injury. One primary focus is on the complement system which serves to recognize danger/injury and initiate signaling pathways for response. A second area of focus is on the intracellular signaling pathways that are involved in the enhancement of phagocytic function. Since the cellular signals generated by phagocytic cells as they ingest specific particles for antigen presentation influence the subsequent immune response, the influence of ligation of these receptors on the generation of immune responses to immunization is also of interest, not only for vaccines against infectious diseases but also for tumor vaccines. Thus, they are investigating the downstream events such as cytokine expression resulting from binding of defense collagens (the prototype of which in our lab is C1q). However, a critical part of all of the studies is the identification of the different subsets of monocyte/macrophages. This is a new, exciting area in which major subsets of macrophages are being defined in terms of surface markers, intracellular enzyme levels and specific functional activities. At least some of these subsets are postulated to be “plastic” and thus capable of “reprogramming” which is particularly exciting. One subset of particular interest is the human equivalent of what has been described as tumor infiltrating macrophages which are sometimes characterized as suppressor macrophages as they do not attack the tumor, but rather may support its survival suppressing cytotoxic activities which should be targeted to the tumor. These studies are in their infancy, but in their efforts to globally characterize functional subsets of the myeloid lineage Dr. Tenner and her colleagues hope to gain tools to distinguish these subsets and to manipulate them for therapeutic benefit.
Selected Publications:
Bohlson, S. S., Silva, R., Fonseca, M. I., and Tenner, A. J. (2005). CD93 is rapidly shed from the surface of human myeloid cells and the soluble form is detected in human plasma. J Immunol 175(2), 1239-47.
Fraser, D. A., Bohlson, S. S., Jasinskiene, N., Rawal, N., Palmarini, G., Ruiz, S., Rochford, R., and Tenner, A. J. (2006). C1q and MBL, components of the innate immune system, influence monocyte cytokine expression. J Leukoc Biol 80(1), 107-16.
Bohlson, S. S., Fraser, D. A., and Tenner, A. J. (2007). Complement proteins C1q and MBL are pattern recognition molecules that signal immediate and long-term protective immune functions. Mol Immunol 44(1-3), 33-43.
Fraser, D. A., Arora, M., Bohlson, S. S., Lozano, E., and Tenner, A. J. (2007). Generation of inhibitory NFkappaB complexes and phosphorylated cAMP response element-binding protein correlates with the anti-inflammatory activity of complement protein C1q in human monocytes. J Biol Chem 282(10), 7360-7.
Pisalyaput, K., and Tenner, A. J. (2008). Complement component C1q inhibits beta-amyloid- and serum amyloid P-induced neurotoxicity via caspase- and calpain-independent mechanisms. J Neurochem 104(3), 696-707. |
