Systems-Oriented Immunology and Inflammation Research

The idea that death can save lives is indeed a truism, but for complex organisms there is a significant protective mechanism in the background. Apoptosis is the name for the “suicide programme”, with which injured, old, mutated or dangerous cells can be deactivated in human tissue. But this suicide program can be misused by pathogens – or it can get out of control. You can read here how scientists are seeking to understand and make use of programmed cellular death in a cooperative research group within the Institute for Molecular and Clinical Immunology at the Otto-von-Guericke University Magdeburg and the HZI.


Selected Publications

Frentzel S, Katsoulis-Dimitriou K, Jeron A, Schmitz I*, Bruder D*. Essential role of IκB(NS) for in vivo CD4(+) T-cell activation, proliferation, and Th1-cell differentiation during Listeria monocytogenes infection in mice. Eur J Immunol. 2019 May 3. doi: 10.1002/eji.201847961 5 [Epub ahead of print].

Plaza-Sirvent C, Schuster M, Neumann Y, Heise U, Pils MC, Schulze-Osthoff K, Schmitz I. (2017) c-FLIP Expression in Foxp3-Expressing Cells Is Essential for Survival of Regulatory T Cells and Prevention of Autoimmunity. Cell Reports 18:12-22.

Neumann Y, Bruns SA, Rohde M, Prajsnar TK, Foster SJ, Schmitz I. (2016) Intracellular Staphylococcus aureus eludes selective autophagy by activating a host cell kinase. Autophagy 12:2069-2084.

Annemann M, Wang Z, Plaza-Sirvent C, Glauben R, Schuster M, Ewald Sander F, Mamareli P, Kühl AA, Siegmund B, Lochner M, Schmitz I. IκBNS Regulates Murine Th17 Differentiation during Gut Inflammation and Infection. J Immunol. 2015 Mar 15;194(6):2888-98.

Schuster M, Glauben R, Plaza-Sirvent C, Schreiber L, Annemann M, Floess S, Kühl AA, Clayton LK, Sparwasser T, Schulze-Osthoff K, Hühn J, Siegmund B, Pfeffer K, Schmitz I. (2012) IκBNS Protein Mediates Regulatory T Cell Development via Induction of the Foxp3 Transcription Factor. Immunity 37:998-1008.   

further publications

Bachelor & Master
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Audio Podcast

  • Gas und Bremse für ImmunantwortenUnser Immunsystem ist geprägt durch ein kompliziertes Wechselspiel unterschiedlicher Immunzellen, das Wissenschaftler stückchenweise verstehen lernen. Um das Immunsystem daran zu hindern, dass es sich gegen uns selbst richtet oder um ihm auch mal einen Schubs geben zu können, müssen sie die molekularen Stellknöpfe finden – und beeinflussen. Einen dieser Stellknöpfe haben Ingo Schmitz und Marc Schuster entdeckt. Folgen Sie den beiden ins Labor...
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