Immunosenescence

Immunosenescence (Latin immunis actually tax-free ', in the figurative sense, unaffected ', ' free ', ' pure ' and lat = senescere, grow old ' ) is the name for the slow deterioration of the immune system in the elderly. One effect of immunosenescence is the increase in infection-related morbidity and mortality in elderly patients.

The term immunosenescence (English immunosenescence ) was coined by the U.S. gerontologist Roy Walford 1969.

Although substantially below the immunosenescence is meant human, this phenomenon is not limited to humans. Most vertebrates, perhaps even all, are affected.

Description

In older people, a number of changes take place in both the innate and adaptive immune system in the ( " acquired immune system "). These age-related changes lead to a decrease in the function of the immune system. This is known as immunosenescence. The immunosenescence can be detected diagnostically by a number of immunological parameters. The state of the innate and adaptive immune defense in the elderly is directly correlated to the health of those affected. In many cases, however, it is unclear how the dysfunction of the immune system is the cause or the effect.

The age-related degradation of the immune system has a direct impact and explains, for example the increased susceptibility of the elderly to infectious diseases, diseases which are associated with inflammatory processes ( such as Alzheimer's and cardiovascular diseases), and autoimmune diseases. This entails both an accelerated aging process as well as increased mortality.

Immunosenescence is a complex developmental process that is more of a restructuring with qualitative changes of parts of the immune system as equivalent to a general decline of all immune functions.

From an evolutionary point of view predominate at a young age, the positive effects of the immune system, for example to combat pathogens to ensure successful reproduction of the organism. Possible negative effects (see also inflammation aging) that occur only after the reproduction phase, could be eliminated by evolution not by selection.

Changes in the immune system in aged

The involution of the thymus begins at puberty. This process is completed between the 40th and 50th year of life. After that, no maturation of T - lymphocytes is possible, so that the immune system is dependent on the existence of the formed up to this point in time T-lymphocytes. At a young age, the body has a high proportion of naive - that is not activated - T lymphocytes, a small proportion of memory cells and effector hardly. In old age, however, is exactly the opposite: it is dominated by the effector memory cells are second and there are hardly naive T lymphocytes present. The decrease in T- and B- lymphocytes in age is called age-related leukopenia. The number of non-specific cytotoxic NK cells, however, increases with age. This reversal of cell conditions has changes in the cytokine result. Interleukin -2 is secreted significantly less than in young age, whereas interleukin -4 and interferon - γ are formed reinforced. This in turn causes, inter alia, a lower maturation of the B lymphocytes, and a reduced production of antibodies. The altered cytokine milieu that minimal proliferation of naive T - lymphocytes and a changed signal transduction via T -cell receptor (TCR) cause in the presentation of new antigens (antigen presentation), the immune system is unable to respond appropriately. B lymphocytes from the CD19 are not as active, in order to deliver antibodies after contact with antigens of age.

Antigen presenting cells, however, are also at an advanced age still fully functional.

Causes

The immune system is a highly complex defense mechanism of the body, in which many factors affect its function. According contributes to a number of different factors to immunosenescence. Some causes are controversial, which is based, among others, that it is often very difficult to determine whether the above- described changes at the cellular level are intrinsic to a cell type or be caused by external influences, or both is the primary cause. The causality - what is cause and what is effect? - Is often unclear. This is especially in the interaction of B lymphocytes with T- lymphocytes of the case, which is crucial for effective immune response. If an element is affected thereby, it immediately changes the function of the other.

As one of the main causes of the cell biological changes that lead to immunosenescence, which is seen " antigen overload" that has acted on the organism during its life span. Permanent inflammatory processes reduce the number of naive T cells. The repertoire of cells, which are able to respond to the antigens of pathogens, decreasing in continuous.

Cytomegalovirus (HCMV) is a biomarker that is associated with immunosenescence. The human immune system is a significant part of his work with the fight or control has this virus, the utilization increases with age.

According to another theory besides the exposure to antigens, the diet in the development of immunosenescence plays an important role. Particular attention will undersupply contribute proteins to immunosenescence. This is also a starting point for possible therapeutic measures.