Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain.
In experimental autoimmune encephalomyelitis (EAE) myelin-specific T lymphocytes attack the myelinated tissue of the central nervous system (CNS). In the Lewis rat, EAE as a rule has an acute, monophasic course. With spontaneous clinical recovery the inflammatory CNS infiltrates are cleared from the nervous tissue within a few days. This is well in line with the remarkably low incidence of myelin-specific T cells present in EAE infiltrate. Combining immunocytochemical techniques, ultrastructural criteria and in situ nick translation we found up to 49% of T lymphocytes in EAE lesions showing signs of apoptosis at the time of recovery from disease. Our results suggest that apoptosis of T lymphocytes may be one possible mechanism to eliminate T lymphocytes from inflammatory brain lesions.
Schmied
M
M
Research Unit of Experimental Neuropathology, Austrian Academy of Sciences, Vienna.
Breitschopf
H
H
Gold
R
R
Zischler
H
H
Rothe
G
G
Wekerle
H
H
Lassmann
H
H
D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000648:ultrastructure*; D016923:Cell Death; D004249:DNA Damage; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000473:pathology* / Q000503:physiopathology; D005821:Genetic Techniques; D007124:Immunoenzyme Techniques; D007958:Leukocyte Count; D051381:Rats; D011917:Rats, Inbred Lew; D017207:Rats, Sprague-Dawley; D013601:T-Lymphocytes / Q000648:ultrastructure*