Univ. Prof. DDr. Christoph Binder
Dept. of Laboratory Medicine
Medical University of Vienna & Center for Molecular Medicine of the Austrian Academy of Sciences
Lazarettgasse 14, AKH BT25.2, 1090 Vienna, Austria
Phone: +43 (0)1 40400 - 73755
Fax: +43 (0)1 40400 - 73588
Know-how and research interests
Dr. Binder is interested in the role of immune mechanisms in atherosclerosis and the immune recognition of oxidation-specific epitopes. His interests are clearly interdisciplinary and span vascular biology, lipid oxidation, natural antibodies and innate immunity. In the past years, Dr. Binder’s research has focused on the role of natural IgM antibodies in atherosclerosis. He first described the atheroprotective role of the natural IgM antibody T15/EO6, which was followed by studies defining protective mechanisms of T15/EO6. This included the demonstration that a large part of natural IgM in mice and humans is directed against oxidation-specific epitopes, and the characterization of germline encoded natural IgM antibodies that are derived from innate B-1 cells. Currently, his laboratory is defining the functional role of natural IgM antibodies using mouse models of atherosclerosis and is working to identify molecular mechanisms that lead to the production of these antibodies by B-1 cells. A particular emphasis is put on identifying ways how these responses can be exploited for atheroprotective interventions. Major efforts focus on the recent discovery that a large part of natural IgM and complement factor H bind malondialdehyde-epitopes and protect against the consequences of oxidative stress. In addition, Dr. Binder’s research interests include the role of circulating microparticles as carriers of biologically active oxidized lipids and as targets of innate immunity.
Christoph Binder focuses on the immune responses that modulate atherosclerosis. Projects aim at the characterization of innate immune responses that mediate the recognition of lipid-peroxidation derived epitopes, and major efforts focus on the characterization of immune responses to malondialdehyde-epitopes. In addition, the role and function of B-cell subsets and natural antibodies specifically are being investigated.
Techniques and infrastructure of the research group
The group utilizes mouse models of atherosclerosis in combination with various immune deficient models for morphometric analyses of the extent of atherosclerosis and assessment of lesion phenotype by immunohistochemistry. Major techniques used include a wide array of immunological assays, flow cytometry, FACSorting, adoptive in vivo cell transfer and bone marrow transplantation; the biochemical generation of oxidized lipid antigens/ligands and standard molecular biology and cell culture techniques. Group members have access to a fully equipped cell culture facility, FACS sorter and analyzers, microtiter plate readers, ultracentrifuge, HPLC, FPLC, PCR equipment (incl. multichannel Real-time PCR), next generation sequencing equipment, cryo- and microtome, and a fluorescent microscope with imaging equipment.
5 selected publications
Cardilo-Reis L, Gruber S, Schreier SM, Drechsler M, Papac-Milicevic N, Weber C, Wagner O, Stangl H, Soehnlein O, Binder CJ. 2012 Interleukin-13 protects from atherosclerosis and modulates plaque composition by skewing the macrophage phenotype. EMBO Mol Med. 4(10):1072-86.
Weismann, D., K. Hartvigsen, N. Lauer, K. L. Bennett, H. P. Scholl, P. Charbel Issa, M. Cano, H. Brandstatter, S. Tsimikas, C. Skerka, G. Superti-Furga, J. T. Handa, P. F. Zipfel, J. L. Witztum, and C. J. Binder. 2011. Complement factor H binds malondialdehyde epitopes and protects from oxidative stress. Nature 478: 76-81.
Chou, M. Y., L. Fogelstrand, K. Hartvigsen, L. F. Hansen, D. Woelkers, P. X. Shaw, J. Choi, T. Perkmann, F. Backhed, Y. I. Miller, S. Horkko, M. Corr, J. L. Witztum, and C. J. Binder. 2009. Oxidation-specific epitopes are dominant targets of innate natural antibodies in mice and humans. J Clin Invest 119: 1335-1349.
Binder, C. J., S. Horkko, A. Dewan, M. K. Chang, E. P. Kieu, C. S. Goodyear, P. X. Shaw, W. Palinski, J. L. Witztum, and G. J. Silverman. 2003. Pneumococcal vaccination decreases atherosclerotic lesion formation: molecular mimicry between Streptococcus pneumoniae and oxidized LDL. Nat Med 9: 736-743.
Binder, C. J., M. K. Chang, P. X. Shaw, Y. I. Miller, K. Hartvigsen, A. Dewan, and J. L. Witztum. 2002. Innate and acquired immunity in atherogenesis. Nat Med 8: 1218-1226.