Replicative senescence is a term for aging cells. Basically it means that cells are not able to replicate as they had been when younger. With advancing age, the immune system experiences replicative senescence. It can no longer produce the cellular responses necessary to fight a pathogen effectively.
This is probably a primary reason that so many elderly persons who are hospitalized contract pneumonia.
Here is more about it.
Rita B. Effros,
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095-1732, USA
Elderly persons have been exposed to a myriad of pathogens over their lifespan. This life-long immunological history leads, in some cases, to the generation of expanded populations of memory CD8 T cells [killer T cells: T cells with CD8 receptors that recognize, e.g., antigens on the surface of a virus-infected cell] that have reached the end stage of replicative senescence.
In cell culture, CD8 T cells that are subjected to repeated rounds of antigen-driven proliferation [cell proliferation that is driven by any foreign material that is specifically bound by a specific antibody or specific lymphocytes] eventually show irreversible cell cycle arrest, permanent and complete loss of CD28 gene expression [(Cluster of Differentiation 28) is the major co-stimulatory receptor molecule required for activation of naïve T cells.], apoptosis resistance, reduced gene transcription of the major stress protein in response to heat shock, and shortened telomeres compared to their CD28-expressing progenitors.
Clinical studies have documented that high proportions of CD8 T cells that lack CD28 are correlated with reduced antibody response to influenza vaccination and are also an immune marker of increased risk of mortality in persons greater than 80 years of age. In addition: CD8 T cells, lacking CD28 expression, have been documented to have suppressive influences on immune function. Thus, senescent CD8 T cells may affect immune function both directly and indirectly by modulating other immune cell types.
The potential role of senescent T cells in bone homeostasis is suggested as a potentially fruitful area for future investigation. The patterns of cytokine changes observed during the progression to senescence in cell culture are consistent with this possibility, and T cells producing these same cytokines have, in fact, been identified within the bone marrow in murine [mouse] models of osteoporosis. Interestingly, CD8 T cells with markers of replicative senescence are correlated with increased osteoporotic fractures in the elderly.
Thus, senescent CD8 T cells are associated with a variety of deleterious health-related outcomes, suggesting that these cells may exert pleiotropic [having multiple effects on the phenotype] negative effects on both immune and non-immune organ systems during aging.
PMID: 15050285. NIH, NLM, PubMed access to MEDLINE
Calorie restriction protects against age-related decline of the immune system. Lower white blood cells, which are common in calorie restricted humans, may indicate less immune challenge and reduced cell proliferation, thus preserving strong immune response for when it is really needed. One food we thought important for improving immune response was fish oil. Now we’ve begun to question that. In part due to the excellent work by Dr. Jenifer Fenton, an expert in how foods affect immunity and cancer risk. She has done some very provocative research on fish oil’s effect on immunity, for example,
Dietary fish oil alters T lymphocyte cell populations and exacerbates disease in a mouse model of inflammatory colitis. Cancer Res. 2010 Oct 15;70(20):7960-9. Woodworth HL, McCaskey SJ, Clinthorne J, Langohr I, Duriancik D, Gardner EM, Fenton JI
So we decided it was essential to invite Dr. Fenton to discuss her work on a LivingTheCRWay.com expert teleconference. You can find out more about the expert teleconference series and how to be part of it here.