Granulocyte and natural killer activity in the elderly

Citation
G. Di Lorenzo et al., Granulocyte and natural killer activity in the elderly, MECH AGE D, 108(1), 1999, pp. 25-38
Citations number
52
Categorie Soggetti
Cell & Developmental Biology
Journal title
MECHANISMS OF AGEING AND DEVELOPMENT
ISSN journal
00476374 → ACNP
Volume
108
Issue
1
Year of publication
1999
Pages
25 - 38
Database
ISI
SICI code
0047-6374(19990401)108:1<25:GANKAI>2.0.ZU;2-A
Abstract
The deterioration of the immune system in ageing, 'immunosenescence', is th ought to contribute to increased morbidity and mortality from infections an d possibly autoimmune diseases and cancer. The most profound changes involv e effector and immunoregulatory T-cell functions. Immunosenescence appears also to be related to changes in non specific immunity as well. In the pres ent study we have assessed superoxide production, chemotaxis and the expres sion of the apoptosis-related molecule APO1/Fas (CD95) on neutrophils (PMN) from young and old subjects. Furthermore, we have measured the basal natur al killer (NK) activity of young and elderly subjects and we have compared the number of CD16 + cells found in these two groups. We observed a signifi cant decrease age-related both of formation of O-2(-) and chemotaxis wherea s no significant correlation between age and the expression of CD95 on gran ulocyte membrane was demonstrated, suggesting that an increase age-related of CD95-linked apoptosis of PMN should be not an important determinant in t he decreased PMN function. We also observed a significant correlation betwe en age and NK activity. The decreased NK cell function was not due to a dec reased number of NK cells in effector cell preparations since the number of CD16 + cells was significantly increased in old subjects. In conclusion, o ur results show that in the elderly there is also a deficit of the aspecifi c immunity that might play a role in the pathogenic mechanisms of the immun osenescence. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.