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(American Journal of Pathology. 1998;153:715-724.)
© 1998 American Society for Investigative Pathology


Regular Articles

T-Cell Apoptosis in Inflammatory Brain Lesions

Destruction of T Cells Does Not Depend on Antigen Recognition

Jan Bauer* , Monika Bradl{dagger} , William F. Hickey{ddagger} , Sonja Forss-Petter* , Helene Breitschopf* , Chris Linington{dagger} , Hartmut Wekerle{dagger} and Hans Lassmann*

From the Institute of Neurology,* University of Vienna, Vienna, Austria; Department of Neuroimmunology,{dagger} Max Planck Institute for Neurobiology, Martinsried, Germany; and Department of Pathology,{ddagger} Dartmouth Medical School, Lebanon, New Hampshire

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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