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Isolation and Transplantation of Different Aged Murine Thymic Grafts.
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Thymic function is maintained during Salmonella-induced atrophy and recovery.

Ewan A Ross1, Ruth E Coughlan, Adriana Flores-Langarica

  • 1Medical Research Council Centre for Immune Regulation, School of Immunity and Infection, Institute for Biomedical Research, Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|September 21, 2012
PubMed
Summary

Systemic Salmonella infection causes severe thymic atrophy, but T cell output is maintained. Thymic function recovers post-infection, ensuring naive T cell numbers are sustained.

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Area of Science:

  • Immunology
  • Microbiology

Background:

  • Thymic atrophy is a common virulence factor in pathogens, potentially reducing T cell output.
  • Proposed causes include increased apoptosis, premature thymocyte egress, or thymic shutdown.

Purpose of the Study:

  • To investigate the relationship between systemic Salmonella infection and thymic function.
  • To determine the impact of thymic atrophy on T cell output during infection.

Main Methods:

  • Studied Salmonella infection in mice.
  • Analyzed thymocyte numbers, T cell maturation, and thymic output.
  • Utilized single-joint TCR rearrangement excision circle analysis.

Main Results:

  • Salmonella infection caused a 50-fold reduction in thymocyte numbers (thymic atrophy).
  • Despite atrophy, naive T cell numbers increased peripherally.
  • Thymic T cell maturation was maintained, with only a modest decrease in recent thymic emigrants.

Conclusions:

  • Thymic atrophy does not necessarily lead to dysfunctional T cell output.
  • Thymic homeostasis adjusts to systemic infection to maintain naive T cell output.
  • Recovery of thymocyte numbers is linked to increased early thymic progenitor activity.