Effect of age on lymphocyte proliferation

McCarron, M.A.; Osborne, Yvonne; Story, Colin; Dempsey, J.; Turner, David R.; Morley, Alexander A.

doi:10.1016/0047-6374(87)90041-8

Cited by 63 publications

(15 citation statements)

References 9 publications

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“…4). This latter feature may be of particular importance in old age, in which T cell responsiveness is diminished [14][15][16] and clonal elimination of T lymphocytes may take place earlier, after a lower number of population doublings [29][30][31]. The well known agerelated decline of immune function [14] may thus be mitigated by DC, which in the course of immune responses may increase T cell proliferation and thus rescue cells otherwise destined to perish [32].…”

Section: Discussionmentioning

confidence: 99%

Morphologically and functionally intact dendritic cells can be derived from the peripheral blood of aged individuals

Steger

Maczek

Grubeck‐Loebenstein

1996

Clinical and Experimental Immunology

128

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SUMMARYDendritic cells are antigen-presenting cells (APC), which are crucial for the initiation of an immune response. In spite of the well known decline of immune function in old age, no information is yet available on whether dendritic cells are also affected by the ageing process. It was therefore the aim of this study to compare peripheral blood dendritic cells (DC) from old and young healthy individuals. Using granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4, DC were propagated from peripheral blood mononuclear cells (PBMC). The obtained cell populations had a typical dendritic morphology and expressed HLA class I and class II, CD23, CD32, CD40, CD44 and CD54, but not CD3 and CD19. Larger numbers of DC were obtained from old individuals than from young ones in spite of a similar expression pattern of surface molecules. DC from aged persons also survived better under in vitro culture conditions. When tested for their antigen-presenting capacity, DC from young and old individuals were equally effective in inducing the proliferation of tetanus toxoid-specific T cell clones after antigenic stimulation. Peripheral blood DC from aged individuals may thus still function as powerful APC. They may represent useful tools for immunotherapy in the aged.

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Section: Discussionmentioning

confidence: 99%

Morphologically and functionally intact dendritic cells can be derived from the peripheral blood of aged individuals

Steger

Maczek

Grubeck‐Loebenstein

1996

Clinical and Experimental Immunology

128

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“…Studies with a histochemical marker suggested that senescent cells may accumulate with age in vivo (147). As in the case of fibroblasts, T cell lines and clones from older individuals typically show a smaller number of population doublings in vitro than observed for cells from younger persons (218,384,604).…”

Section: Replicative Senescence As a Putative Consequence Of Redoxmentioning

confidence: 99%

Free Radicals in the Physiological Control of Cell Function

Dröge

2002

Physiological Reviews

8,454

5,836

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At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish “redox homeostasis.” Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman ( J Gerontol 11: 298–300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.

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“…118 Similarly, T lymphocytes possess a limited in vitro lifespan corresponding to replicative senescence. 119 Aging may be considered as the consequence of several cellular metabolic modifications occurring at different levels such as cell cycle and telomeric length regulation, structural organization, cellular interactions, stress response capability, and catabolic functions among which autophagy is grouped.…”

Section: Immunosenescence: a Particular Example Of Consequences Of Aumentioning

confidence: 99%

Autophagy and Aging: The Importance of Maintaining "Clean" Cells

et al. 2005

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Previously published online as an Autophagy E-publication: http://www.landesbioscience.com/journals/autophagy/abstract.php?id=2017 KEY WORDS Review Autophagy and AgingThe Importance of Maintaining "Clean" Cells ABSTRACTA decrease in the turnover of cellular components and the intracellular accumulation of altered macromolecules and organelles are features common to all aged cells. Diminished autophagic activity plays a major role in these age-related manifestations. In this work we review the molecular defects responsible for the malfunctioning of two forms of autophagy, macroautophagy and chaperone-mediated autophagy, in old mammals, and highlight general and cell-type specific consequences of dysfunction of the autophagic system with age. Dietary caloric restriction and antilipolytic agents have been proven to efficiently stimulate autophagy in old rodents. These and other possible experimental restorative efforts are discussed.

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Effect of age on lymphocyte proliferation

Cited by 63 publications

References 9 publications

Morphologically and functionally intact dendritic cells can be derived from the peripheral blood of aged individuals

Morphologically and functionally intact dendritic cells can be derived from the peripheral blood of aged individuals

Free Radicals in the Physiological Control of Cell Function

Autophagy and Aging: The Importance of Maintaining "Clean" Cells

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