Yersinia pseudotuberculosis supports Th17 differentiation and limits de novo regulatory T cell induction by directly interfering with T cell receptor signaling.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
AbstractAdaptive immunity critically contributes to control acute infection with enteropathogenic Yersinia pseudotuberculosis; however, the role of CD4(+) T cell subsets in establishing infection and allowing pathogen persistence remains elusive. Here, we assessed the modulatory capacity of Y. pseudotuberculosis on CD4(+) T cell differentiation. Using in vivo assays, we report that infection with Y. pseudotuberculosis resulted in enhanced priming of IL-17-producing T cells (Th17 cells), whereas induction of Foxp3(+) regulatory T cells (Tregs) was severely disrupted in gut-draining mesenteric lymph nodes (mLNs), in line with altered frequencies of tolerogenic and proinflammatory dendritic cell (DC) subsets within mLNs. Additionally, by using a DC-free in vitro system, we could demonstrate that Y. pseudotuberculosis can directly modulate T cell receptor (TCR) downstream signaling within naïve CD4(+) T cells and Tregs via injection of effector molecules through the type III secretion system, thereby affecting their functional properties. Importantly, modulation of naïve CD4(+) T cells by Y. pseudotuberculosis resulted in an enhanced Th17 differentiation and decreased induction of Foxp3(+) Tregs in vitro. These findings shed light to the adjustment of the Th17-Treg axis in response to acute Y. pseudotuberculosis infection and highlight the direct modulation of CD4(+) T cell subsets by altering their TCR downstream signaling.
CitationYersinia pseudotuberculosis supports Th17 differentiation and limits de novo regulatory T cell induction by directly interfering with T cell receptor signaling. 2017 Cell. Mol. Life Sci.
AffiliationHelmholtz Centre for infection research, Inhoffenstr.7, 38124 Braunschweig, Germany.
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
- Impact of CCR7 on T-Cell Response and Susceptibility to Yersinia pseudotuberculosis Infection.
- Authors: Pezoldt J, Pisano F, Heine W, Pasztoi M, Rosenheinrich M, Nuss AM, Pils MC, Prinz I, Förster R, Huehn J, Dersch P
- Issue date: 2017 Sep 15
- CCR2<sup>+</sup> Inflammatory Monocytes Are Recruited to Yersinia pseudotuberculosis Pyogranulomas and Dictate Adaptive Responses at the Expense of Innate Immunity during Oral Infection.
- Authors: Zhang Y, Khairallah C, Sheridan BS, van der Velden AWM, Bliska JB
- Issue date: 2018 Mar
- CD8(+) T cells restrict Yersinia pseudotuberculosis infection: bypass of anti-phagocytosis by targeting antigen-presenting cells.
- Authors: Bergman MA, Loomis WP, Mecsas J, Starnbach MN, Isberg RR
- Issue date: 2009 Sep
- Superantigenic Yersinia pseudotuberculosis induces the expression of granzymes and perforin by CD4+ T cells.
- Authors: Goubard A, Loïez C, Abe J, Fichel C, Herwegh S, Faveeuw C, Porte R, Cayet D, Sebbane F, Penet S, Foligné B, Desreumaux P, Saito H, Sirard JC, Simonet M, Carnoy C
- Issue date: 2015 May
- A protective epitope in type III effector YopE is a major CD8 T cell antigen during primary infection with Yersinia pseudotuberculosis.
- Authors: Zhang Y, Mena P, Romanov G, Lin JS, Smiley ST, Bliska JB
- Issue date: 2012 Jan