Latz, Eicke

Eicke Latz

Bonn, Germany

Eicke Latz studied medicine in Göttingen and Berlin and worked as an intensive care physician at the Charité Hospital in Berlin. Starting in 2000, he received post-doctoral training at Boston University and UMass Medical School, joining the UMass faculty in 2006. In 2010, he returned to Germany and founded the Institute of Innate Immunity at the University of Bonn.

 

Eicke has co-founded IFM Therapeutics, DiosCure Therapeutics, and a ‘Stealth’ biotech that translate discoveries into novel therapeutics. He has been a highly cited scientist in immunology yearly since 2014, and he has received prestigious awards, such as the Gottfried Wilhelm Leibniz Prize in 2018.


Monday 23 May

Vascular response in atherosclerosis: From epigenetics to bone marrow

Chair:
  • Alberico Catapano
  • Kausik Ray

Epigenetic control is one of the most fundamental regulatory systems within the cell. Although different cells contain the same genetic material, they have different epigenomic signatures, which may be heritable or temporary, caused by dynamic responses to the environment thereby providing a link between phenotypic profile and disease risk. Epigenetic modifications, such as DNA methylation and post-translational histone processing, have emerged as important regulators of key signalling pathways that alter monocyte/macrophage phenotypes in response to environmental stimuli, and thus important factors in the pathogenesis of atherosclerosis. In contrast to adaptive immune responses, epigenetic reprogramming of transcriptional pathways mediates trained immunity, involving enhanced responsiveness to subsequent triggers. This process is likely to confer detrimental outcomes in the context of chronic inflammatory diseases, such as atherosclerosis.

Atherosclerotic plaque formation is a dynamic multi-cellular process in which the activity of the different cell types involved is essentially determined by the regulation of different genes. Epigenetic factors modulate vascular smooth muscle cell phenotype to either promote or prevent arterial remodelling. These insights have led to suggestions that atherosclerosis is an epigenetic disorder rather than a ‘lipid’, ‘metabolic’, and ‘inflammatory’ disorder. The ongoing challenge is to understand how the mechanisms of epigenetic regulation, including those mediated by intragenic epigenetic modifications and long coding RNAs, promote vascular disease. Finally, the reversibility of epigenetic modifications may suggest future potential for identifying novel therapeutic targets for atherosclerosis.

Key references

Budden CF, Gearing LJ, Kaiser R, Standke L, Hertzog PJ, Latz E. Inflammasome-induced extracellular vesicles harbour distinct RNA signatures and alter bystander macrophage responses. J Extracell Vesicles 2021;10(10):e12127.

Latz E. The inflammasome: from bench to bedside. Nat Rev Immunol 2021;21:622-623.

Divangahi M, Aaby P, Khader SA, Barreiro LB, Bekkering S, Chavakis T, van Crevel R, Curtis N, DiNardo AR, Dominguez-Andres J, Duivenvoorden R, Fanucchi S, Fayad Z, Fuchs E, Hamon M, Jeffrey KL, Khan N, Joosten LAB, Kaufmann E, Latz E, Matarese G, van der Meer JWM, Mhlanga M, Moorlag SJCFM, Mulder WJM, Naik S, Novakovic B, O’Neill L, Ochando J, Ozato K, Riksen NP, Sauerwein R, Sherwood ER, Schlitzer A, Schultze JL, Sieweke MH, Benn CS, Stunnenberg H, Sun J, van de Veerdonk FL, Weis S, Williams DL, Xavier R, Netea MG. Trained immunity, tolerance, priming and differentiation: distinct immunological processes. Nat Immunol 2021;22:2-6