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  • Author or Editor: B. Stercz x
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The sharp increase of life expectancy and the increasing ratio of ageing population pose new challenges for the public health system. The elderly suffer from more frequent and severe infections than young people. Theoretically, vaccination could protect the elderly against several infectious diseases, but due to their age-related immune impairment, vaccination might fail in many cases. Instead of ineffective vaccination campaigns, exploration and restoration of age-dependent dysregulation of their immune functions have to be placed into the focus of recent research. Frequent comorbidities in these people augment immune defects. Immunosenescence affects both the innate and adaptive immunity. Disturbances in macrophage-derived cytokine release and reduction of the natural killer cell mediated cytotoxicity lead to increased frequency of respiratory, gastrointestinal and skin infections. Although the humoral immunity retains most of its original activity through life span, ageing dampens the ability of B cells to produce antibodies against novel antigens. Age-related declination of the cellular immunity is the consequence of thymic atrophy, reduced output of new T lymphocytes, accumulation of anergic memory cells, deficiencies in the cytokine production and uncertain antigen presentation. Persistent infection by different herpesviruses and other parasites contribute to the loss of immunosurveillance and premature exhaustion of T cells.

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One of the greatest health-care challenges in the elderly is to ensure that vaccination against infections are optimally effective, but vaccination can only be effective if cells that are capable of responding are still present in the repertoire. The reversing of immunosenescence could be achieved by improving immune responses or altering vaccine formulation. Recent vaccination strategies in the elderly exert low effectiveness. Nutritional interventions and moderate exercise delay T cell senescence. Telomerase activity and expression of toll-like receptors can be improved by chemotherapy. Reversion of thymic atrophy could be achieved by thymus transplantation, depletion of accumulated dysfunctional naive T cells and herpesvirus-specific exhausted memory cells. Administration of immunostimulatory and anti-inflammatory cytokines show the best practical approach. Reduced dendritic cell activity and co-receptor expression might be increased by interleukin (IL)-2 administration. IL-7 protects both B and T lymphocytes, but IL-2, IL-10, keratinocyte growth factor, thymic stromal lymphopoietin, as well as leptin and growth hormone also have a stimulatory effect on thymopoiesis. In animals, several strategies have been explored to produce more efficacious vaccines including high dose vaccines, DNA vaccines with immunostimulatory patch, virosomal vaccines and vaccines containing new adjuvants. Hopefully, one of these approaches will be translated into human therapy in a short time.

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