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Severe colitis in mice with aberrant thymic selection

G A Holländer1, S J Simpson, E Mizoguchi

  • 1Division of Pediatric Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.

Immunity
|July 1, 1995
PubMed
Summary
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T cell development in Tg epsilon 26 mice leads to colitis. Normal thymic development prevents this inflammation, suggesting aberrant T cell selection causes disease.

Area of Science:

  • Immunology
  • Developmental Biology
  • Gastroenterology

Background:

  • Tg epsilon 26 mice exhibit early T cell development arrest, impacting thymic stromal cells.
  • Previous studies showed wild-type bone marrow can restore fetal, but not adult, Tg epsilon 26 thymic microenvironments.

Purpose of the Study:

  • To investigate the consequences of T cell reconstitution in adult Tg epsilon 26 mice.
  • To determine if T cells selected in an abnormal thymus induce colitis.
  • To explore preventative strategies for colitis in this model.

Main Methods:

  • Bone marrow transplantation into adult Tg epsilon 26 mice.
  • Engraftment of fetal Tg epsilon 26 thymus followed by bone marrow transplantation.
  • Analysis of T cell populations and colon inflammation.

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Main Results:

  • T cell-reconstituted adult Tg epsilon 26 mice developed a wasting syndrome with severe colon inflammation (colitis).
  • Activated CD4+ T cells from the thymus infiltrated the colon, driving colitis.
  • Bone marrow-transplanted mice with a fetal Tg epsilon 26 thymus did not develop colitis.

Conclusions:

  • T cells selected in an aberrant thymic microenvironment can induce severe colitis.
  • Normal thymic development is crucial for preventing colitis by generating protective T cells.
  • This model highlights the link between thymic T cell selection and inflammatory bowel disease.