Emmy Noether Junior Research Group

The immune system possesses elegant strategies to cope with potential harmful invading microorganisms. Nevertheless, pathogens themselves have evolved mechanisms to deal with the threats imposed by the immune system. Yeasts like Candida species are common commensals of the human microbiota, yet also major opportunistic fungal pathogens that frequently cause superficial and even fatal infections. The commensal co-existence with the human host allows the co-evolution of fungal adaptation strategies in line with the threats imposed by the host.

While the competing microbiota is potentially the major challenge for host-associated Candida species during commensalism, the immune system is the major threat that can compromise the survival during infection. The fungus, therefore, employs strategies to evade immune recognition or even escape the immune cells after it has been attacked. A constant expression of these pathogenicity strategies is not efficient and may also jeopardize the commensal lifestyle of these pathogens. An adaptive regulation is essential to only engage these pathogenicity strategies when needed. We investigate the adaptations induced by host conditions (like temperature) and host molecules. In particular, we are interested in the underlying molecular mechanisms inducing these adaptations and the host proteins the fungus may sense to do so.

Further related topics dealing with immunotherapy and interaction with the microbiota are investigated in close collaboration with the Department of Microbial Pathogenicity Mechanisms.


Mark Gresnigt


Alonso-Roman R, Mosig AS, Figge MT, Papenfort K, Eggeling C, Schacher FH, Hube B#, Gresnigt MS (2024) Organ-on-chip models for infectious disease research. Nat Microbiol 9(4), 891-904.
Jaeger M, Dietschmann A, Austermeier S, Dinçer S, Porschitz P, Vornholz L, Maas RJA, Sprenkeler EGG, Ruland J, Wirtz S, Azam T, Joosten LAB, Hube B, Netea MG, Dinarello CA, Gresnigt MS (2024) Alpha1-antitrypsin impacts innate host-pathogen interactions with Candida albicans by stimulating fungal filamentation. Virulence 15(1), 2333367.
Kaden T*, Alonso-Roman R*, Akbarimoghaddam P*, Mosig AS, Graf K, Raasch M, Hoffmann B, Figge MT#, Hube B#, Gresnigt MS# (2024) Modeling of intravenous caspofungin administration using an intestine-on-chip reveals altered Candida albicans microcolonies and pathogenicity. Biomaterials 307, 122525.


The research group is funded by the German Research Foundation (DFG)within the Emmy Noether Programme of the  (project number 434385622 / GR 5617/1-1) and the Collaborative Research Centre (CRC)/Transregio (TRR) 124 “FungiNet” (DFG project number 210879364). The group is further supported by a strategic Basic Research (SBO) grant the Research Foundation Flanders (FWO) and a Boehringer Ingelheim Foundation Exploration Grant.