In vitro induction of activation-induced cell death in lymphocytes from chronic periodontal lesions by exogenous Fas ligand

Citation
T. Sawa et al., In vitro induction of activation-induced cell death in lymphocytes from chronic periodontal lesions by exogenous Fas ligand, INFEC IMMUN, 67(3), 1999, pp. 1450-1454
Citations number
20
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
67
Issue
3
Year of publication
1999
Pages
1450 - 1454
Database
ISI
SICI code
0019-9567(199903)67:3<1450:IVIOAC>2.0.ZU;2-E
Abstract
Periodontitis is a chronic inflammatory disease which gradually destroys th e supporting tissues of the teeth, leading to tooth loss in adults, The les ions are characterized by a persistence of inflammatory cells in gingival a nd periodontal connective tissues. To understand what mechanisms are involv ed in the establishment of chronic lesions, we hypothesized that infiltrati ng lymphocytes might be resistant to apoptosis. However, both Bcl-2 and Bcl -xL were weakly detected in lymphocytes from the lesions, compared with tho se from peripheral blood, suggesting that these cells are susceptible to ap optosis, Nevertheless, very few apoptotic cells were observed in tissue sec tions from the lesions. Lymphocytes from the lesions expressed mRNA encodin g Fas, whereas Fas-ligand mRNA was very weakly expressed in lymphocytes fro m the lesions and in periodontal tissues. Since the results indicated that lymphocytes in the lesions might be susceptible to Fas-mediated apoptosis b ut lack the death signal, we next investigated if these lymphocytes actuall y undergo apoptosis by the addition of anti-Fas antibodies in vitro. Fas-po sitive lymphocytes from the lesions underwent apoptosis by these antibodies , but Fas-negative lymphocytes and Fas-positive peripheral lymphocytes did not undergo apoptosis by these antibodies. These results indicate that lymp hocytes in the lesions are susceptible to activation-induced cell death and are induced to die by apoptosis after the addition of exogenous Fas ligand .