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Repertoire-dependent immunopathology.

Joshua Milner1, Jerrold Ward, Andrea Keane-Myers

  • 1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Journal of Autoimmunity
|September 25, 2007
PubMed
Summary
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A limited T-cell repertoire in mice led to severe eosinophilic inflammation and disease. This highlights the critical role of T-cell diversity in preventing inflammatory conditions.

Area of Science:

  • Immunology
  • Inflammation Research

Background:

  • Limited T-cell receptor repertoire and lymphopenia in humans are linked to severe eosinophilic inflammatory diseases.
  • A mouse model was developed to investigate the impact of T-cell repertoire size on immune responses.

Purpose of the Study:

  • To investigate the role of T-cell repertoire size in the development of eosinophilic inflammatory diseases.
  • To determine the impact of regulatory T-cells (Tregs) and effector T-cells on Th2-mediated pathology.

Main Methods:

  • C57BL/6 Rag2-/- mice received either a limited (30,000) or large (2 million) number of CD4 T-cells.
  • Mice were analyzed 3-5 months post-transfer for inflammatory markers, including pneumonia, eosinophilia, IgE levels, and airway hyperresponsiveness.
  • The role of CD25+ CD4 Tregs was assessed by depletion and pretreatment strategies.

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Main Results:

  • Mice receiving limited T-cells developed severe macrophage pneumonia, eosinophilia, elevated IgE, and airway hyperresponsiveness.
  • Donor T-cells were enriched for IL-4, IL-5, and IL-13 production, indicating a Th2-biased response.
  • Depletion of Tregs exacerbated Th2 pathology, while pretreatment with a sufficient number of Tregs prevented disease development.

Conclusions:

  • Limited T-cell repertoire complexity, particularly in Tregs, can impair the control of immunopathologic responses.
  • Reduced diversity in effector T-cells may contribute to the development of Th2-mediated phenotypes and severe eosinophilic inflammation.