ROLE OF APOPTOSIS IN EXPERIMENTAL ALLERGI C ENCEPHALOMYELITIS AND HUNTINGTONS-DISEASE

Citation
H. Villarroya et F. Eclancher, ROLE OF APOPTOSIS IN EXPERIMENTAL ALLERGI C ENCEPHALOMYELITIS AND HUNTINGTONS-DISEASE, La Semaine des hopitaux de Paris, 73(15-16), 1997, pp. 492-495
Citations number
9
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00371777
Volume
73
Issue
15-16
Year of publication
1997
Pages
492 - 495
Database
ISI
SICI code
0037-1777(1997)73:15-16<492:ROAIEA>2.0.ZU;2-R
Abstract
Apoptosis or programmed cell death contributes significantly to the re gulation of animal cell populations under physiologic conditions, in c ontrast to necrosis which is pathological cell death. A distinctive pa ttern of DNA fragmentation demonstrable using the Tunel technique is s een in apoptosis. In a study performed in rats with EAE, we found apop totic cells (expression of Fas and Fast) among not only CD4(+) lymphoc ytes and macrophages but also among neurones and glial cells during th e recovery phase of the illness. Also, the proinflammatory cytokine TN Falpha was expressed at a high level during the acute phases of EAE an d subsequently persisted after the recovery phase. These results sugge st that TNFalpha may contribute to the induction of apoptosis via a me chanism involving ACTH and glucocorticoids. Apoptotic death of striata l neurones has been reported in Huntington's disease.