Age- and gender-related values of lymphocyte subsets in subjects from Northern and Southern Italy.
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Journal Article↗
Biomedical subjects
G Scialabba
Publications and source records attributed to G Scialabba.
Early activation of gammadelta T lymphocytes in the elderly.
T cell function is altered in vivo and in vitro in elderly compared with young subjects, and this alteration is believed to contribute to morbidity and mortality in man due to the greater incidence of infection, as well as autoimmunity and cancer in elderly. The majority of T cells express TCRalphabeta whereas TCRgammadelta is expressed on a minority of T cells. Moreover, it is known that gammadelta T lymphocytes display major histocompatibility complex (MHC)- unrestricted cytotoxicity that is reminiscent of natural killer (NK) activity. In view of earlier findings on both T cells and NK cells in the elderly, we hypothesised a different behaviour of gammadelta T lymphocytes from old subjects when compared with gammadelta T lymphocytes obtained from young people. Therefore, to gain further insight into mechanisms of immunosenescence in this little-studied population, we studied immunofluorescence analysis gammadelta T cells from the elderly. Our preliminary results show that the percentage of blood gammadelta T cells in lymphocytes from old subjects is decreased when compared with the young. Interestingly, these cells are more activated in the elderly than in young subjects; expression of CD69, an early activation marker, is increased in gammadelta T lymphocytes from old subjects after three hours of in vitro culture both with and without lipopolysaccharide stimulation. Thus, our findings, which need confirmation, strongly suggest that, in humans, gammadelta T cells are early responders when compared with alphabeta T cells. They may act as 'first aid' cells to replace the described deficit of the specific and aspecific immunity in elderly. In this view, the proinflammatory status, observable in the elderly, renders them ready to be stimulated by exogenous agents.
Adult↗
Apoptosis and ageing.
Stimulation of T cells from aged individuals leads to different kinds and/or size of responses if compared with the responses of T cells obtained from young individuals. In fact elderly is associated with a progressive decline of immune response besides an increasing incidence of autoimmune phenomena. These differences might be the result of modified cellular mechanisms controlling the immune system in the course of ageing. The apoptotic deletion of activated T cells has been proposed as the key mechanism to maintain T cell homeostasis, and in this respect CD95 (Fas antigen) seems to play a major role in this course of events. In this study we show that just collected lymphocytes from old subjects displayed an increased expression of the apoptosis molecule CD95. The expression of CD95 and the spontaneous apoptosis showed the same trend. In fact the percentage of apoptotic cells in blood collected from old subjects was enhanced too. The lymphocyte subpopulation analysis by flow cytometry did not show significant changes in T subset percentages between old and young subjects. Moreover mononuclear cells obtained from aged individuals underwent apoptosis in culture in response to a single stimulation with mitogen or anti-CD3, more than mononuclear cells from young controls. To gain insight into mechanisms of this increased apoptosis, experiments were performed to evaluate the behaviors of lymphocytes from old and young donors in respect of interleukin-2 (IL-2) rescue from apoptosis. Results show that IL-2 rescued only a little fraction of cells of old donors from apoptosis when activated by anti-CD3 and that this effect was not related to a different expression of CD95. Thus, during the course of ageing the different regulation of T cell homeostasis might be also explained by the modified proneness of lymphocytes to undergo apoptosis. The contemporaneous demonstration of a reduced Ca2+ influx in lymphoid cells of these subjects allows to suppose that multiple defects play a role in the pathogenesis of immunosenescence.
Adult↗