Ageing and immunity

Boraschi, Diana; Giudice, Giuseppe Del; Dutel, Catherine; Ivanoff, B; Rappuoli, Rino; Grubeck‐Loebenstein, Beatrix

doi:10.1016/j.vaccine.2010.03.035

Cited by 55 publications

(14 citation statements)

References 26 publications

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“…Alzheimer's disease results in chronic white matter degeneration, much like MS, yet an inflammatory MS-like disorder is not triggered in this situation. One explanation may be “immune senescence”, whereby immune responsiveness is known to wane with age [72]. The decreasing intensity of lymphocytic infiltration with age in the MS brain [33], despite continuing demyelination and neurodegeneration, is consistent with this suggestion.…”

Section: Reconstructing Ms: a Thought Experimentsmentioning

confidence: 60%

Pathoetiology of multiple sclerosis: are we barking up the wrong tree?

Stys

2013

F1000Prime Rep

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Despite a century of intensive investigation, the underlying cause of multiple sclerosis has eluded us. It is clear that there exists a prominent progressive degenerative phenotype together with an important autoimmune inflammatory component, and careful histopathological examination always shows, to a greater or lesser degree, concomitant degeneration/demyelination and adaptive T cell-dependent immune responses. Given this picture, it is difficult, if not impossible, to definitively say whether degeneration or autoimmunity is the initiator of the disease. In this review, I put forward the evidence for and against both models and speculate that, in contrast to the accepted view, it is equally likely that multiple sclerosis may be a degenerative disease that secondarily elicits an autoimmune response, and suggest how this might influence therapeutic approaches.

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Section: Reconstructing Ms: a Thought Experimentsmentioning

confidence: 60%

Pathoetiology of multiple sclerosis: are we barking up the wrong tree?

Stys

2013

F1000Prime Rep

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“…This immune senescent profile has been considered of immunological risk for infections and shown to be an independent predictor of death in aged subjects (29). Moreover, it resembles the profile of immunosenescence documented in individuals thymectomized early in life during corrective cardiac surgery (26, 30, 31).…”

Section: Discussionmentioning

confidence: 99%

Major CD4 T-Cell Depletion and Immune Senescence in a Patient with Chronic Granulomatous Disease

et al. 2017

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Chronic granulomatous disease (CGD) results from primary defects in phagocytic reactive oxygen species (ROS) production. T-cell evaluation is usually neglected during patients’ follow-up, although T-cell depletion has been reported in CGD through unknown mechanisms. We describe here a 36-year-old patient with X-linked CGD with severe CD4 T-cell depletion <200 CD4 T-cells/μl, providing insights into the mechanisms that underlie T-cell loss in the context of oxidative burst defects. In addition to the typical infections, the patient featured a progressive T-cell loss associated with persistent lymphocyte activation, expansion of interleukin (IL)-17-producing CD4 T-cells, and impaired thymic activity, leading to a reduced replenishment of the T-cell pool. A relative CD4 depletion was also found at the gut mucosal level, although no bias to IL-17-production was documented. This immunological pattern of exhaustion of immune resources favors prompt, potentially curative, therapeutic interventions in CGD patients, namely, stem-cell transplantation or gene therapy. Moreover, this clinical case raises new research questions on the interplay of ROS production and T-cell homeostasis and immune senescence.

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“…Aging represents a complex remodeling in which innate and adaptive immune responses deteriorate, leading to greater susceptibility to infectious diseases and reduced responses to vaccination [1]. Aging is characterized by increased levels of circulating pro-inflammatory cytokines, such as TNF-α and IL-6 [2–4], which have been associated with functional disability/mortality of the elderly.…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus (CMV) seropositivity decreases B cell responses to the influenza vaccine

Frasca

Diaz

Romero

et al. 2015

Vaccine

105

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Cytomegalovirus (CMV)-seropositivity has been shown to have a negative effect on influenza vaccine-specific antibody responses. In this paper we confirm and extend these results showing for the first time a negative association between CMV-seropositivity and B cell predictive biomarkers of optimal vaccine responses. These biomarkers are switched memory B cells and AID in CpG-stimulated B cell cultures measured before vaccination which positively correlate with the serum response to the influenza vaccine. We also found that CMV-seropositivity is associated with increased levels of B cell-intrinsic inflammation and these both correlate with lower B cell function. Finally, CMV-seropositivity is associated with decreased percentages of individuals responding to the vaccine in both young and elderly individuals.

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Ageing and immunity

Cited by 55 publications

References 26 publications

Pathoetiology of multiple sclerosis: are we barking up the wrong tree?

Pathoetiology of multiple sclerosis: are we barking up the wrong tree?

Major CD4 T-Cell Depletion and Immune Senescence in a Patient with Chronic Granulomatous Disease

Cytomegalovirus (CMV) seropositivity decreases B cell responses to the influenza vaccine

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