The Innate Immune System: Defining Molecular Mechanisms of Host Defense
Our research is centered on defining the molecular mechanisms of the response of the innate immune system to infection. This research is focused on investigating how products of microbial pathogens activate cells to express new genes. Currently our major efforts are on identification of cell surface receptors that recognize products of microbial pathogens and on elucidation of intracellular signaling pathways responsible for transmitting information from the cell surface to the nucleus. This research utilizes molecular, cellular and structural biological approaches. While focused on specific problems of biomedical importance, our research also impacts general areas of cell biology that include the understanding of how GPI-anchored cell surface receptors function and how intracellular kinase cascades are regulated and how such kinase cascades modulate cell function.
Ph.D. (Immunology), University of Pennsylvania 1971
Aderem, A. and Ulevitch, R.J. Toll-like receptors in the induction of the innate immune response. Nature 406:782-787, 2000.
Arbibe, L., Mira, J.-P., Kline, L., Godowski, P.J., Ulevitch, R.J. and Knaus, U.G. Tolllike receptor 2-mediated NF-kB activation requires a Rac1-dependent pathway. Nature Immunol. 1:533-540, 2000.
Werts, C., Tapping, R.I., Mathison, J.C., Chuang, T.-H., Kravchenko, V. V., Saint Girons, I., Haake, D., Godowski, P.J., Hayashi, F., Ozinsky, A.,. Underhill, D., Aderem, A., Tobias, P.S. and Ulevitch, R.J. Leptospiral endotoxin activates cells via a TLR2dependent mechanism. Nature Immunol. 2:346-352, 2001.
Ge, B., Gram, H., Di Padova, F., Huang, B., New, L., Ulevitch, R., Luo Y., and Han, J. MAP kinase-independent activation of p38a mediated by TAB 1-dependent autophosphorylation of p38a. Science 295:1291-1294, 2002.