Fabio Re, PHD
In this section
Fabio Re graduated from the University of Milan in 1989. In the lab of Dr. Alberto Mantovani at the Mario Negri Institute for Pharmacological Research he conducted studies on the role of the Interleukin-1 receptor type II that led to the concept of “decoy receptor”, a paradigm later found to apply to other cytokine systems.
In 1994 he moved to Columbia University, New York, in the lab of Dr. Jeremy Luban where he studied the effect of HIV infection on cell cycle progression.
In 1999 he joined the lab of Dr. Jack Strominger at the Dana-Farber Cancer Institute, Boston, where he studied several aspects of the biology of toll-like receptors (TLR), including the differential activation of dendritic cells by TLR agonists and the interaction of LPS with TLR4/MD-2. During this period he held an Instructor position in the Department of Pathology of the Harvard Medical School.
In 2004 he was appointed Assistant Professor in the Department of Molecular Sciences at the University of Tennessee Health Science Center in Memphis. His research efforts remained focused on innate immunity. He was tenured and promoted to Associate Professor in 2010.
In 2012 he joined the Department of Microbiology and Immunology of Chicago Medical School at Rosalind Franklin University of Medicine and Science as Associate Professor with Tenure.
Fabio serves as grant reviewer for the National Institute of Health, the National Science Foundation, and the Welcome Trust. He is Associate Editor for The Journal of Immunology and reviewer for several immunological journals.
Our lab studies the interaction of the host with pathogens and commensals. We focus our attention on inflammation and innate immune pathways activated in response to infection or vaccination. Particular attention is devoted to Toll-like receptors (TLR) and Nod-like receptors (NLR), the tissue injury caused by unrestrained neutrophils activation, and the role of “innate” B1 B cells. These processes are investigated using animal models of infection with the NAID Select Agents Francisella tularensis and Burkholderia pseudomallei.
Re Lab Protocols
del Barrio L., Sahoo M., Lantier L., Reynolds J.M., Ceballos-Olvera I., Re F. (2015) Production of anti-LPS IgM by B1a B cells depends on IL-1β and is protective against lung infection with Francisella tularensis LVS. PLoS Pathog 11(3): e1004706. doi:10.1371/journal.ppat.1004706
Sahoo, M., del Barrio, L., Miller, M.A., and Re, F. (2014) Neutrophil elastase causes tissue damage that decreases host tolerance to lung infection with Burkholderia species. PLoS Pathog. 10(8): e1004327. doi:10.1371/journal.ppat.1004327. PMID:25166912
Ceballos-Olvera, I., Sahoo, M., Miller, M. A., Barrio, L., and Re, F. (2011) Inflammasome-dependent Pyroptosis and IL-18 Protect Against Burkholderia pseudomallei Lung Infection While IL-1b Is Deleterious. PLoS Pathog 7(12): e1002452. doi:10.1371/journal.ppat.1002452
Sahoo, M., Ceballos-Olvera, I., Barrio, L. and Re, F. (2011) Role of the inflammasome, IL-1b, and IL-18 in bacterial infections. ScientificWorldJournal 11:2037-2050
Madan Lala, R., Peixoto K.V., Re, F., Rengarajan J. (2011) Mycobacterium tuberculosis Hip1 dampens macrophage pro-inflammatory responses by limiting TLR2 activation. Infect. Immun. 79:4828-4838
Jayakar, H., Parvathreddy, J., Fitzpatrick, E. A., Bina, X. R., Bina, J. E., Re, F., Emery, F. D., and Miller, M.A. (2011) A galU mutant of Francisella tularensis is attenuated for virulence in a murine pulmonary model of tularemia. BMC Microbiol. 11:179
Tsukahara, T., Tsukahara, R., Fujiwara, Y., Yue, J., Cheng, Y., Guo, H., Bolen, A., Zhang, C., Balazs, L., Re, F., Du, G., Frohman, M. A., Baker, D. L., Parrill, A. L., Uchiyama, A., Kobayashi, T., Murakami-Murofushi, K., and Tigyi, G. (2010) Phospholipase D2-dependent Inhibition of the Nuclear Hormone Receptor PPARγ by Cyclic Phosphatidic Acid. Molec. Cell 39:421-432
Re, F. (2010) Inflammasome activation by pathogenic crystals and particles. Prog. Inflamm. Res. (Martinon, F., Couillin, I., Petrilli, V., eds) (in press)
Li, H., Ambade, A., and Re, F. (2009) Cutting Edge: Necrosis activates the NLRP3 inflammasome. J. Immunol. 183:1528-1532
Li, H., Willingham, S. B., Ting, J. P.-Y., and Re, F. (2008) Cutting Edge: Inflammasome activation by Alum and Alum’s adjuvant effect are mediated by NLRP3.J. Immunol. 181:17-21
Nance, S.C., Yi, A.K., Re, F., Fitzpatrick, E.A.(2008) MyD88 is necessary for neutrophil recruitment in hypersensitivity pneumonitis. J. Leukoc. Biol. 83:1207-17
Thakran, S., Li, H., Lavine, C.L., Miller, M. A., Bina, J. E., Bina, X. R., Re, F. (2008) Identification of Francisella tularensis lipoproteins that stimulate the Toll-like receptor (TLR) 2/TLR1 heterodimer. J. Biol. Chem. 283:3751-3760
Li, H., Nooh, M.M., Kotb, M., and Re, F. (2008) Commercial peptidoglycan preparations are contaminated with superantigen-like activity that stimulates IL-17 production. J. Leuk. Biol. 83:409-418
Li, H., Nookala, S., and Re, F. (2007) Alum Adjuvants Activate Caspase-1 And Induce IL-1b And IL-18 Release. J. Immunol. 178:5271-5276. (68)· Teghanemt, A., Re, F., Prohinar, P., Widstrom, R., Gioannini, T. L., and Weiss, J. P. (2007). Novel roles in human MD-2 of phenylalanine 121 and 126 and tyrosine 131 in activation of Toll-like Receptor 4 by endotoxin. J. Biol. Chem. 283:1257-1266
Cao, F., Castrillo, A., Tontonoz, P., Re, F., Byrne, G.I. (2006) Chlamydia pneumoniae-induced Macrophage Foam Cell Formation Is Mediated by Toll-Like Receptor 2. Infect Immun. 75:753-759
Prohinar, P., Re, F., Widstrom, R., Zhang, D., Teghanemt, A., Weiss, J. P., and Gioannini, T. L. (2006) Specific high affinity interactions of monomeric endotoxin: protein complexes with Toll-like receptor 4 ectodomain. J. Biol. Chem. 282:1010-1017
Li, H, Nookala, S., Bina, X. W., Bina, J. E., and Re, F. (2006) Innate immune response to Francisella tularensis is mediated by TLR2 and caspase-1 activation.J. Leuk. Biol. 80: 766-773