Protrait Latz

Prof. Dr. Eicke Latz

Cooperation Unit Leader
Prof. Latz is Director of  Institute of Innate Immunity at the University of Bonn

German Center for Neurodegenerative Diseases (DZNE)

c/o Institute of Innate Immunity
Biomedical Centre (BMZ), 1G007
University Hospital
University of Bonn

Sigmund-Freud-Str. 25

53127 Bonn

+ 49 (0) 228 287 51223
+ 49 (0) 228 287 51221

Group members
Name Phone
Dr. Igor Kitanovic, Postdoc +49 (0) 228 / 287-51220
Further group members (Uni Bonn/third party funding)  
Anne Alfter, Technical Assistant +49 (0) 228 / 287-51225
Damien Bertheloot, PhD Student +49 (0) 228 / 287-51227
Dr. Christine De Nardo, Scientific Coordinator +49 (0) 228 / 287-51236
Dr. Dominic De Nardo, Postdoc +49 (0) 228 / 287-51225
Gudrun Engels, Technical Assistant +49 (0) 228 / 287-51220
Dr. Bernardo Franklin, Postdoc +49 (0) 228 / 287-51225
Simon Görgen, PhD Student +49 (0) 228 / 287-51229
Alena Grebe, PhD Student +49 (0) 228 / 287-51220
Dr. Gabor Horvath, Postdoc +49 (0) 228 / 287-51229
Larisa Labzin, PhD Student +49 (0) 228 / 287-51220
Dr. Pia Langhoff, Postdoc +49 (0) 228 / 287-51225
Brian Monks, PhD Student +49 (0) 228 / 287-51229
Karin Pelka, PhD Student +49 (0) 228 / 287-51227
Andrea Schlichting, Administrative Officer +49 (0) 228 / 287-51239
Rainer Stahl, Senior Technical Assistant +49 (0) 228 / 287-51229
James Stunden, PhD Student +49 (0) 228 / 287-51227
Andrea Stutz, PhD Student +49 (0) 228 / 287-51227
Curriculum vitae

Eicke Latz has studied Medicine at the Georg-August University Göttingen and at the Free University of Berlin and obtained his doctorate in 2001 from the Humboldt University of Berlin. He carried out his postdoctoral work from 2001-2003 in the Golenbock laboratory at the University of Massachusetts Medical School, USA. In 2003 he was awarded an Assistant Research Professorship and in 2006 an Assistant Professorship at the Division on Infectious Diseases, UMass Medical School, which he still holds today. In 2007 he founded, and co-directed the UMass NanoMedicine Institute. He is currently the Director of the Institute of Innate Immunity, at the University of Bonn, Germany, which he established in 2009 when he was recruited back to Germany and awarded a full professorship (W3).

Among his major scientific achievements are the discovery that the NLRP3 inflammasome is activated in brains of patients with Alzheimer’s, and that aggregates of amyloid beta mediate neuroinflammation and cognitive decline in murine models of Alzheimer’s disease (Nature 2013); The discovery of the role of cholesterol crystals in atherosclerotic inflammation (Nature 2010); The discovery of the AIM2 inflammasome (Nature 2009); The discovery that lysosomal damage is sensed by the NLRP3 inflammasomes (Nature Immunology 2009); The identification of the activation mechanism of TLR9 (Nature Immunol 2007); and the discovery of the intracellular location of TLR9 and its recruitment from the ER to the endosome (Nature Immunology 2004).

In addition to his research, reviewer, editorial and teaching commitments, Eicke Latz is a member of several advisory boards with strong ties to industry partners. He is affiliated with the Norwegian University of Science and Technology (Trondheim, Norway), is a founder and member of the International Innate Immunity Consortium (IIIC), and he is a member of the ImmunoSensation Cluster of Excellence as well as the Center for Infection Research (DZIF) in Bonn, Germany.

Eicke Latz is the recipient of the GlaxoSmithKline Clinical Science Award (2011), the Dana Foundation Award (2009), the Federation of Clinical Immunology Societies Award (2004), and a Postdoctoral Training Grant of the German Academic Exchange Program (DAAD) (2001). Furthermore, together with the Department of Infectious Diseases at UMass Medical School, Eicke Latz is involved in organizing the Toll Meeting series which focus on all aspects of innate immunity, from basic research to clinical translation.

Selected publications

Activation and regulation of inflammasomes.

Latz E, Xiao S, Stutz A (2013). Nat Rev Immunol. In press

NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice.

Heneka MT*, Kummer MP, Stutz A, Delekate A, Schwartz S, Vieira-Saecker A, Griep A, Axt D, Remus A, Tzeng TC, Gelpi E, Halle A, Korte M, Latz E* and Golenbock DT* (2013). Nature. Jan 31;493(7434):674-8.

Cutting Edge: FAS (CD95) Mediates Noncanonical IL-1beta and IL-18 Maturation via Caspase-8 in an RIP3-Independent Manner.

Bossaller L, Chiang PI, Schmidt-Lauber C, Ganesan S, Kaiser WJ, Rathinam VA, Mocarski ES, Subramanian D, Green DR, Silverman N, Fitzgerald KA, Marshak-Rothstein A* and Latz E* (2012). Journal of immunology, 189(12), 5508-5512.

NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals.

Duewell P, Kono H, Rayner KJ, Sirois CM, Vladimer G, Bauernfeind FG, Abela GS, Franchi L, Nunez G, Schnurr M, Espevik T, Lien E, Fitzgerald KA, Rock KL, Moore KJ, Wright SD, Hornung V, Latz E (2010). Nature 464: 1357-61

Intracellular DNA recognition.

Hornung V and Latz E. (2010). Nat Rev Immunol. 10 (2): 123-130           

AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC.

Hornung V, Ablasser A, Charrel-Dennis M, Bauernfeind F, Horvath G, Caffrey DR, Latz E* & Fitzgerald KA*. (2009). Nature, 458(7237): 514-518.

Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression.

Bauernfeind FG, Horvath G, Stutz A, Alnemri ES, MacDonald K, Speert D, Fernandes-Alnemri T, Wu J, Monks BG, Fitzgerald KA, Hornung V, Latz E (2009). J Immunol 183: 787-91

Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization.

Hornung V, Bauernfeind F, Halle A, Samstad EO, Kono H, Rock KL, Fitzgerald KA*, Latz E* (2008). Nat Immunol 9: 847-56

The NALP3 inflammasome is involved in the innate immune response to amyloid-beta.

Halle A, Hornung V, Petzold GC, Stewart CR, Monks BG, Reinheckel T, Fitzgerald KA, Latz E, Moore KJ, Golenbock DT. (2008). Nat Immunol 9: 857-65

Ligand-induced conformational changes allosterically activate Toll-like receptor 9.

Latz E, Verma A, Visintin A, Gong M, Sirois CM, Klein DC, Monks BG, McKnight CJ, Lamphier MS, Duprex WP, Espevik T, Golenbock DT. (2007). Nat Immunol 8: 772-9

TLR9 signals after translocating from the ER to CpG DNA in the lysosome.

Latz E, Schoenemeyer A, Visintin A, Fitzgerald KA, Monks BG, Knetter CF, Lien E, Nilsen NJ, Espevik T, Golenbock DT. (2004). Nat Immunol 5: 190-8

*These authors contributed equally

The full list of publications is found here.

Areas of investigation/research focus

The innate immune system responds to microbial products and host factors that arise during tissue damage and metabolic dysregulation. Innate immune activation is important for the control of infections and overactivation can lead to inflammatory disease states. An international group of scientists work together with the major aims of:

  • elucidating how the innate immune system maintains health and under which circumstances it promotes diseases
  • using basic research to decipher the molecular mechanisms of innate immune activation
  • developing novel therapeutic approaches that target a multitude of inflammatory diseases, such as Alzheimer's disease, diabetes, and atherosclerosis

The cooperation partner's homepage can be found here.