2007
DOI: 10.1016/j.exger.2007.05.001
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No Immune Risk Profile among individuals who reach 100 years of age: Findings from the Swedish NONA immune longitudinal study

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Cited by 189 publications
(134 citation statements)
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References 20 publications
(21 reference statements)
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“…Among the clinical consequences of the immunosenescence are an increase in the frequency of infectious diseases (and, possibly, an increase in cancer and autoimmune diseases) (Yoshikawa 2000;Strindhall et al 2007) and poor response to vaccines (Gruver et al 2007). The loss of peripheral blood naive T cells is the bestknown effect of immunosenescence and the absence of response to vaccines has been ascribed, at least in part, to this decline (Aspinall et al 2007;Gruver et al 2007).…”
Section: Introductionmentioning
confidence: 99%
“…Among the clinical consequences of the immunosenescence are an increase in the frequency of infectious diseases (and, possibly, an increase in cancer and autoimmune diseases) (Yoshikawa 2000;Strindhall et al 2007) and poor response to vaccines (Gruver et al 2007). The loss of peripheral blood naive T cells is the bestknown effect of immunosenescence and the absence of response to vaccines has been ascribed, at least in part, to this decline (Aspinall et al 2007;Gruver et al 2007).…”
Section: Introductionmentioning
confidence: 99%
“…This concept lends itself to the argument that immunosenescence is not merely a measurement of chronological age but points towards immune exhaustion arising at different ages (i.e., physiological age) (Lang et al 2010b;Mitchell et al 2010). The downward trajectory of an individual's thymic output profile over time has been demonstrated previously by Kilpatrick et al (2008) and could be considered as part of longitudinal studies similar to the OCTA and NONA studies to investigate further the potential role of sj-TREC as predictive marker of aging (Wikby et al 2005;Strindhall et al 2007;Wikby et al 2008). Thus, whether predicting human phenotypes from genotypes is relevant both for personalized medicine and applying preventive strategies (Janssens and van Duijn 2008), additional clinical and translational studies at population, clinical, cellular, and molecular levels are still needed in order to elucidate the exact implications of the TREC values on the age-related senescence of the cell-mediated immune response (Lang et al 2011a).…”
Section: Could We Identify Different Trends Of Aging When Analyzing Smentioning
confidence: 86%
“…Since the single preceding event in all cases of immunosenescence is thymic involution ), can we identify a specific T cell-mediated immunity makers which are linked to a state of immunosenescence? The pioneering OCTO and NONA studies have resulted in the emerging concept of an immune risk profile (IRP) (Wikby et al 2005;Strindhall et al 2007;Wikby et al 2008). This immune condition consists of (1) ) T cells, and T cell proliferative index.…”
Section: Is T Cell-mediated Immunity Senescence a Quantifiable Disorder?mentioning
confidence: 99%
“…Complementarily, findings from the NONA immune longitudinal study confirmed the importance of the IRP as a major predictor of mortality and suggested that survival to the age of 100 years was associated with the selection of individuals with "inverted" IRP that was stable across the time (i.e. avoidance of inverted CD4+/CD8+ ratio and low numbers of CD8+ CD28− T-cells) (Strindhall et al, 2007). However, concerning individuals with a senescent immune system, a better understanding of the age-associated alterations to immunity is still necessary for helping to identify aged individuals requiring specific or additional care during or in prevention of the influenza specific season.…”
Section: How To Identify Individuals Who Are Poor Respondersmentioning
confidence: 89%
“…An alternative method has been to identify the immune risk profile (IRP), a condition consisting of high CD8+, low CD4+ numbers, characterised by an inverted CD4+/CD8+ ratio and a poor mitogen response to concanavalin A (ConA) stimulation and, associated with persistent CMV infection leading to the expansion of dysfunctional terminally differentiated CD8+ CD28− T-cells Strindhall et al, 2007). Interestingly, in an examination of immune parameters over the adult lifespan as a whole, Wikby et al (2008) have observed (i) an increase in the prevalence of individuals having an IRP from about 8% in the age range of 20-59 years to about 16% in the age range of 60-94 years of age, (ii) a higher mortality rate in individuals above 60 years of age who have an CD4+/CD8+ inverted ratio, and (iii) a significant lowering of the numbers of CD3+, CD3+ CD4+ and CD3+ CD8+, and of CD8+ CD45RA+ CCR7+ cells across the adult lifespan.…”
Section: How To Identify Individuals Who Are Poor Respondersmentioning
confidence: 99%