Senescence is a normal biological process that occurs in all organisms and involves a decline in cell functions. This process is caused by molecular regulatory machinery alterations, and it is closely related to telomere erosion in chromosomes. In the context of the immune system, this phenomenon is known as immunosenescence and refers to the immune function deregulation. Therefore, functions of several cells involved in the innate and adaptive immune responses are severely compromised with age progression (e.g., changes in lymphocyte subsets, decreased proliferative responses, chronic inflammatory states, etc.). These alterations make elderly individuals prone to not only infectious diseases but also to malignancy and autoimmunity. This review will explore the molecular aspects of processes related to cell aging, their importance in the context of the immune system, and their participation in elderly SLE patients. 1. Introduction Aging can be defined as the progressive decay of tissue functions which eventually results in organ dysfunction and death. This decline may be the result of the loss of postmitotic cell function or the lack of replacement of such cells due to a decreased stem cell ability to maintain cell division and replication [1]. If the organism suffers damage and it is irreparable, the senescence or aging process will take place by limiting the cells’ proliferative potential. Some control mechanisms include differential gene expression which may be detrimental [2]. However, there is a renewal mechanism that ensures damaged cell replacement. This singular mechanism corresponds to a set of proliferating precursor cells that provide a source of cell replacement within the tissues. The immune system provides an interesting case of replacement: cells that die by apoptosis are replaced by new ones, a process which is essential for immune system longevity and for adequate functionality. This review will describe main molecular mechanisms implicated in immunosenescence and their relationship with autoimmune disease, particularly related to systemic lupus erythematous (SLE). 2. Aging Molecular Mechanisms One of the most striking features of cell aging is its close relationship with telomere length [3]. There is an inverse relationship between telomere length and cellular aging; for example, very short telomeres force their cells to enter senescence. Human telomeres contain guanine-rich repetitive sequences (i.e., TTAGGG) which are gradually lost in each mitotic division. This occurs by the fact that the DNA polymerase is unable to replicate
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