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  • team
  • department
  • center
  • program_project
  • nrc
  • whocc
  • project
  • software
  • tool
  • patent
  • Administrative Staff
  • Assistant Professor
  • Associate Professor
  • Clinical Research Assistant
  • Clinical Research Nurse
  • Clinician Researcher
  • Department Manager
  • Dual-education Student
  • Full Professor
  • Honorary Professor
  • Lab assistant
  • Master Student
  • Non-permanent Researcher
  • Nursing Staff
  • Permanent Researcher
  • Pharmacist
  • PhD Student
  • Physician
  • Post-doc
  • Prize
  • Project Manager
  • Research Associate
  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
  • Director of Institute
  • Director of National Reference Center
  • Group Leader
  • Head of Facility
  • Head of Operations
  • Head of Structure
  • Honorary President of the Departement
  • Labex Coordinator
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← Go to Research

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Starting Date
14
Sep 2015
Status
Ongoing
Members
3
Structures
1

About

The role of innate response of CD8 memory T cell during infections is now well established. However, while the mechanisms that govern its induction and mode of actions in particular IFNg secretion are more and more elucidated, little is known about the regulation of this response.To address this issue, we have established mice models of Salmonella typhimurium (ST) infection, in which we were able to follow the fate of unrelated memory CD8 T cells. These models allowed us to show the consistent and reproducible death of the memory CD8 T cells upon infection. Using different strains of KO mice we could show the dependence of this process on Bcl-2 expression and could exclude type IFN as mediator of this process. The death of non-cognate memory CD8 T cells during the ST infection was associated with a decrease in the level of IFNg measured both in spleen and in the serum of infected mice. The mechanism of this process, its potential role in the regulation of the CD8 innate response and its physiological relevance during the infection is currently under investigation, and will be assessed in other infections.

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