ArticlePloS one2019
Molecular crypsis by pathogenic fungi using human factor H. A numerical model.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Molecular Mimicry Mapping inPathogens (Basel, Switzerland) · 2023Article
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Trends in mathematical modeling of host-pathogen interactions.Cellular and molecular life sciences : CMLS · 2020Review
- Multiscale Solutions to Quantitative Systems Biology Models.Frontiers in molecular biosciences · 2019Article
- A computational model for the evaluation of complement system regulation under homeostasis, disease, and drug intervention.PloS one · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Molecular mimicry is the formation of specific molecules by microbial pathogens to avoid recognition and attack by the immune system of the host. Several pathogenic Ascomycota and Zygomycota show such a behaviour by utilizing human complement factor H to hide in the blood stream. We call this type of mimicry molecular crypsis. Such a crypsis can reach a point where the immune system can no longer clearly distinguish between self and non-self cells. Thus, a trade-off between attacking disguised pathogens and erroneously attacking host cells has to be made. Based on signalling theory and protein-interaction modelling, we here present a mathematical model of molecular crypsis of pathogenic fungi using the example of Candida albicans. We tackle the question whether perfect crypsis is feasible, which would imply that protection of human cells by complement factors would be useless. The model identifies pathogen abundance relative to host cell abundance as the predominant factor influencing successful or unsuccessful molecular crypsis. If pathogen cells gain a (locally) quantitative advantage over host cells, even autoreactivity may occur. Our new model enables insights into the mechanisms of candidiasis-induced sepsis and complement-associated autoimmune diseases.
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