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T-cell apoptosis in inflammatory brain lesions: destruction of T cells does not depend on antigen recognition.

Authors
  • Bauer, J
  • Bradl, M
  • Hickley, W F
  • Forss-Petter, S
  • Breitschopf, H
  • Linington, C
  • Wekerle, H
  • Lassmann, H
Type
Published Article
Journal
The American journal of pathology
Publication Date
Sep 01, 1998
Volume
153
Issue
3
Pages
715–724
Identifiers
PMID: 9736022
Source
Medline
License
Unknown

Abstract

Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes.

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