The heat shock proteins in cellular aging: is zinc the missing link?
T-cell functions are critical for the efficiency of the adaptive immune response. It is now clear that aging is associated with changes in the T-cell response to antigenic stimulation, one of the many changes collectively resulting in immune senescence. Several hypotheses have been proposed to explain such changes. We believe that chronic stimulation of T-cells enhances the appearance of apoptosis-resistant anergic dysfunctional cells; in humans in vivo these are predominantly specific for antigens of persistent viruses, especially CMV. Concomitantly, age-associated zinc deficiency is common and one hypothesis is that lack of zinc bioavailability contributes to impaired T-cell function. This could further compromise the integrity of T-cells under chronic antigenic stress, which can be modelled in long-term clonal cultures in vitro. Newly synthesized heat-shock proteins (HSPs) protect the cellular proteins from degradation under such conditions. In this short review we will briefly outline the role of heat-shock proteins and zinc deficiency in aging in order to finally discuss our own results in the context of a link between HSPs, aging and zinc.
Larbi
Anis
A
Center for Medical Research, Tüebingen Aging and Tumor Immunology group, University of Tüebingen, Waldhornlestrasse 22, 72072, Tüebingen, Germany. anis.larbi@medizin.uni-tuebingen.de
Kempf
Juergen
J
Wistuba-Hamprecht
Kilian
K
Haug
Constantin
C
Pawelec
Graham
G
D000375:Aging / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D016922:Cellular Senescence; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D015032:Zinc / Q000378:metabolism*
D006360:Heat-Shock Proteins; D015032:Zinc