CECAD Microsite


Inflammation is a response of the immune system that aims to defend the organism from pathogens and to promote wound healing and tissue regeneration in response to injury and infection. However, excessive or prolonged inflammation causes tissue damage and is involved in the pathogenesis of a plethora of inflammatory diseases. Chronic inflammation is also implicated in cancer development as well as in ageing and ageing-associated pathologies. Therefore, inflammatory responses need to be tightly regulated to ensure effective host defence and injury repair while preventing excessive tissue pathology and disease. This fine balance between the beneficial and potentially detrimental sides of inflammation is critical for the maintenance of tissue homeostasis and organismal health. Our research aims to understand the mechanisms that regulate inflammation and the pathogenesis of inflammation-related diseases, ultimately aspiring to develop better therapeutic approaches. 

Selected publications

Eftychi C, Schwarzer R, Vlantis K, Wachsmuth L, Basic M, Wagle P, Neurath MF, Becker C, Bleich A, Pasparakis M. (2019) Temporally Distinct Functions of the Cytokines IL-12 and IL-23 Drive Chronic Colon Inflammation in Response to Intestinal Barrier Impairment. Immunity 51: 367-380

Polykratis A, Martens A, Eren RO, Shirasaki Y, Yamagishi M, Yamaguchi Y, Uemura S, Miura M, Holzmann B, Kollias G, Armaka M, van Loo G, Pasparakis M (2019). A20 prevents inflammasome-dependent arthritis by inhibiting macrophage necroptosis through its ZnF7 ubiquitin-binding domain. Nat. Cell Biol. 21: 731-742

Lin J, Kumari S, Kim C, Van T-M, Wachsmuth L, Polykratis A & Pasparakis M (2016). RIPK1 counteracts ZBP1-mediated necroptosis to inhibit inflammation. Nature, 540: 124-128

Vlantis K, Wullaert A, Polykratis A, Kondylis V, Dannappel M, Schwarzer R, Welz P, Corona T, Walczak H, Weih F, Klein U, Kelliher M & Pasparakis M (2016) NEMO Prevents RIP Kinase 1-Mediated Epithelial Cell Death and Chronic Intestinal Inflammation by NF-κB-Dependent and -Independent Functions. Immunity 44: 553–567

Kondylis V, Polykratis A, Ehlken H, Ochoa-Callejero L, Straub BK, Krishna-Subramanian S, Van T-M, Curth H-M, Heise N, Weih F, Klein U, Schirmacher P, Kelliher M & Pasparakis M (2015) NEMO Prevents Steatohepatitis and Hepatocellular Carcinoma by Inhibiting RIPK1 Kinase Activity-Mediated Hepatocyte Apoptosis. Cancer Cell 28: 582–598

Dannappel M, Vlantis K, Kumari S, Polykratis A, Kim C, Wachsmuth L, Eftychi C, Lin J, Corona T, Hermance N, Zelic M, Kirsch P, Basic M, Bleich A, Kelliher M & Pasparakis M (2014) RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis. Nature 513: 90–94

Welz PS, Wullaert A, Vlantis K, Kondylis V, Fernandez-Majada V, Ermolaeva M, Kirsch P, Sterner-Kock A, van Loo G, Pasparakis M (2011) FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation. Nature 477: 330-334

Bonnet MC, Preukschat D, Welz PS, van Loo G, Ermolaeva MA, Bloch W, Haase I, Pasparakis M (2011) The Adaptor Protein FADD Protects Epidermal Keratinocytes from Necroptosis In Vivo and Prevents Skin Inflammation. Immunity 35: 572-582

Nenci A, Becker C, Wullaert A, Gareus R, van Loo G, Danese S, Huth M, Nikolaev A, Neufert C, Madison B, Gumucio D, Neurath MF, Pasparakis M (2007) Epithelial NEMO links innate immunity to chronic intestinal inflammation. Nature 446(7135): 557-561

Luedde T, Beraza N, Kotsikoris V, van Loo G, Nenci A, De Vos R, Roskams T, Trautwein C, Pasparakis M (2007) Deletion of NEMO/IKKgamma in liver parenchymal cells causes steatohepatitis and hepatocellular carcinoma. Cancer Cell 11(2): 119-132

For full list of publications click here:

New CRC 1403 "Cell Death in Immunity, Inflammation and Disease

CRC1403 focuses on cell death and its role in immunity and disease. Cell death is a fundamental biological process for multicellular organisms, traditionally viewed as a process safeguarding tissue homeostasis by counterbalancing cell proliferation. This view has dramatically changed during the last years by the identification of different genetically controlled cellular death programs and the realisation that these cell death pathways contribute to immunity and disease. Accumulating evidence revealed that dying cells communicate with bystander cells triggering tissue responses that could be protective by mediating tissue repair but could also cause tissue damage and disease. A new concept has now emerged, in which cell death is an integral component of the organismal response to stress caused by microbial and non-microbial insults that is important for both protective immunity and the pathogenesis of immune-related diseases. The overarching goal of the CRC 1403 is to explore how diverse forms of cell death are regulated and how they contribute to health and disease in animals and plants, with particular focus on immunity, inflammation and host-microbe interactions. The CRC1403 includes projects from scientists from the MNF and the Medical faculty of the UoC, together with scientists from the MPI for Plant Breeding Research and the MPI for Ageing Research and groups from the University of Bonn and the LMU in Munich. The CRC also provides a link between the Excellence Clusters CECAD and CEPLAS in Cologne as well as the EC Immunosensation in Bonn.


Spokesperson: Manolis Pasparakis

Deputy Spokesperson: Hamid Kashkar



"Temporally Distinct Functions of the Cytokines IL-12 and IL-23 Drive Chronic Colon Inflammation in Response to Intestinal Barrier Impairment"

Congratulations to Christina, Laurens and Robin!



"A20 prevents inflammasome-dependent arthritis by inhibiting macrophage necroptosis through its ZnF7 ubiquitin-binding domain"

Congratulations to Apostolos and Onur!  

SharedIt link: : https://rdcu.be/bBCOk