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Updated: Aug 19, 2026
Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses
Published on: November 16, 2016
Yersinia outer protein P inhibits CD8 T cell priming in the mouse infection model
Konrad Trülzsch1, Gernot Geginat, Thorsten Sporleder
1Max von Pettenkofer Institut für Hygiene und Medizinische Mikrobiologie, Ludwig Maximilians Universität, München, Germany. truelzsch@m3401.mpk.med.uni-muenchen.de <truelzsch@m3401.mpk.med.uni-muenchen.de>
Abstract:
Pathogenic yersiniae translocate a mixture of effector proteins called Yersinia outer proteins (Yops) into the cytosol of eukaryotic cells by their type III secretion system. YopP is one of the best characterized of these effector proteins and known to inhibit the proinflammatory response of the host by interfering with NF-kappaB signal transduction and inducing apoptosis of macrophages. The effects of YopP on the immune response were studied by a Yersinia Ag-independent approach using bacteria that translocate the well-characterized model Ag listeriolysin O of Listeria monocytogenes via their type III secretion system. In this study we demonstrate a novel function for YopP in vivo. It is shown for the first time that YopP not only counteracts the innate immune defense but also inhibits the adaptive immune system by suppressing the development of an effective CD8 T cell response in a mouse model. A possible mechanism for this could be the inhibition of Ag presentation by dendritic cells (DC). In vitro this is shown to be due to the rapid induction of programmed DC death and to inhibition of DC maturation. Using this approach we could further show that the listeriolysin O-specific CD8 T cells generated in vivo by the yopP mutant are functional and are able to protect mice against a lethal challenge with wild type Listeria.
Insights
Yersinia outer protein P (YopP) inhibits both innate and adaptive immunity. This study shows YopP suppresses CD8 T cell responses by impairing dendritic cell function, impacting host defense against infection.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Pathogenic Yersinia species deliver effector proteins (Yops) into host cells via type III secretion systems.
- YopP is a key Yersinia effector known to inhibit host inflammatory responses and induce macrophage apoptosis.
- Understanding YopP's full impact on host immunity requires Yersinia antigen-independent investigation.
Purpose of the Study:
- To investigate the in vivo effects of YopP on the adaptive immune system.
- To elucidate the role of YopP in suppressing CD8 T cell responses.
- To determine the impact of YopP on dendritic cell function and maturation.
Main Methods:
- Utilized a Yersinia antigen-independent system expressing listeriolysin O via a type III secretion system.
- Assessed CD8 T cell responses in a mouse model challenged with bacteria expressing YopP.
- Investigated dendritic cell (DC) maturation and apoptosis in vitro upon YopP exposure.
Main Results:
- YopP was found to inhibit the development of effective CD8 T cell responses in vivo.
- YopP induced rapid apoptosis and inhibited maturation of dendritic cells in vitro.
- CD8 T cells generated in the absence of YopP were functional and provided protection against Listeria challenge.
Conclusions:
- YopP actively suppresses the adaptive immune system, specifically CD8 T cell immunity, in addition to innate defenses.
- Impaired dendritic cell function is a key mechanism by which YopP inhibits adaptive immunity.
- Targeting YopP or its mechanisms could enhance host immune responses against Yersinia infections.
