Relationship between Aging and the Immune System

B cells from aged mice exhibit reduced apoptosis upon B-cell antigen receptor stimulation and differential ability to up-regulate survival signals

“…Thus, elderly individuals experience a higher incidence of several diseases such as autoimmune disorders and infections than younger individuals [1][2][3]. In this sense, deficiencies in the humoral and cell-mediated immune response have been reported during ageing [4,5].…”

Changes in the Human Thymus During Aging

“…Their rationales range from explaining aging by a committed progressive breakdown of functions of immunocompetent cells and their clonal exhaustion (WALFORD 1969;BURNET 1970;HOLLIDAY et al 1981) to explaining progressive loss of immunity by phenomena of aging such as: (a) somatic mutation (ORGEL 1963(ORGEL , 1973; (b) error in replication or repair of DNA (JOHNSON and STREHLER 1972;HART and SETLOW 1974); (c) error proneness of DNA polymerases and related enzymes (BURNET 1976); respiration-dependent injury to the mitochondrial genome (FLEMING et al 1982) in other cells than immunocompetent cells. Several excellent recent reviews have compiled mutual associations between age and immune system of different species, including man (WALFORD 1969;MAKINODAN et al 1971 ;KAY and MAKINO-DAN 1976;MAKINODAN and YUNIS 1977;YUNIS et al 1978;GOOD et al 1979;KISHIMOTO and MITSUYA 1980;WILLIAMS et al 1980;LEECH 1980;WEKSLER 1980;MAKINODAN 1980;KAY and MAKINODAN 1981). In particular, T cell system-dependent immune functions seem to decline with age (Table 1), whereas functions of macrophages and B cells do not appear to be impaired KAY and MAKINODAN 1981;BENNER et al 1981).…”

“…Several excellent recent reviews have compiled mutual associations between age and immune system of different species, including man (WALFORD 1969;MAKINODAN et al 1971 ;KAY and MAKINO-DAN 1976;MAKINODAN and YUNIS 1977;YUNIS et al 1978;GOOD et al 1979;KISHIMOTO and MITSUYA 1980;WILLIAMS et al 1980;LEECH 1980;WEKSLER 1980;MAKINODAN 1980;KAY and MAKINODAN 1981). In particular, T cell system-dependent immune functions seem to decline with age (Table 1), whereas functions of macrophages and B cells do not appear to be impaired KAY and MAKINODAN 1981;BENNER et al 1981). ALBRIGHT and MAKINODAN (1966), MAKI-NODAN et al (1971) a TYAN (1976TYAN ( ,1977 GHESCHLAGHI (1977), LUSCIETI et al (1980) a KAyet al (1979) KAY (1979a, ALDER et al (1982 KISHIMOTO et al (1978), GUPTA and GOOD (1979), ONSRUD (1981) MASCART-LEMONE et al (1982), VAN DE GRIEND et al (1982) JAMIL and MILLARD (1981) HALLGREN et al (1983), VAN DE GRIEND et al (1982) a OLSSON and CLAESSON (1973) a CHEN (1971CHEN ( ,1974 a OGDEN and MICKLEM (1976) a GILMAN et al (1981) a Popp (1977) GROSS ( 1965), WALDORF (1968), MACKAY (1972), …”

“…In particular, T cell system-dependent immune functions seem to decline with age (Table 1), whereas functions of macrophages and B cells do not appear to be impaired KAY and MAKINODAN 1981;BENNER et al 1981). ALBRIGHT and MAKINODAN (1966), MAKI-NODAN et al (1971) a TYAN (1976TYAN ( ,1977 GHESCHLAGHI (1977), LUSCIETI et al (1980) a KAyet al (1979) KAY (1979a, ALDER et al (1982 KISHIMOTO et al (1978), GUPTA and GOOD (1979), ONSRUD (1981) MASCART-LEMONE et al (1982), VAN DE GRIEND et al (1982) JAMIL and MILLARD (1981) HALLGREN et al (1983), VAN DE GRIEND et al (1982) a OLSSON and CLAESSON (1973) a CHEN (1971CHEN ( ,1974 a OGDEN and MICKLEM (1976) a GILMAN et al (1981) a Popp (1977) GROSS ( 1965), WALDORF (1968), MACKAY (1972), MEIER et al (1975), CZLONKOWSKA and KORLAK (1979), BUCKLEY and WHITE (1979), ApOSTOLOFF et al (1980) a STUTMAN et al (1968), FRIEDMAN et al (1974), HERON (1981) BACH (1977), BECKER et al (1979) PAWELEC et al (1983 a STJERNSWARD (1966), PERKINS and CACHEIRO (1977), …”

T‐lymphocyte subpopulation changes during hemolysis in glucose‐6‐phosphate dehydrogenase (G6PD)‐deficient children

“…Another could be that the OKT4/OKT8 inverted ratio is related to a massive engagement of the immune system by the very high number of altered red blood cells. As occurs during the ageing process of normal red blood cells [5], it is theoretically possible that the red blood cell damage leading to hemolysis provokes the exposure of new antigens on the membrane surface. This excessive antigenic load may temporarily reduce the number of OKT4-positive cells and increase the OKT8-positive cells, thus causing a diminished OKT4/OKT8 ratio.…”