**Author details**

*Thymus*

Without regard to the nature of its invading pathogens, the infected thymus may encounter atrophy and architectural changes. The infected thymus is consequently liable to induce apoptosis, pathogen-specific immune responses, T cells that are

Less is understood for mechanisms of thymic escape from infection and/or survival after being infected. However, it is suggested that the thymus may be affected by seeding of cells from other peripheral sites of infection. Therefore, elimination of infection from other peripheral sites might help in the prevention of seeding and development of infection in the thymus. When it gets infected, there is evidence on the presence of antigen-specific CD4+ or CD8+ T cells of other peripheral organs. This would imply that the thymus might in time profit from responses mediated by

Older individuals have higher rates of diseases, e.g., infections, malignancies, and autoimmune diseases, demonstrate lower responsiveness to vaccines, and are less capable of immune restoration following chemotherapy, radiotherapy, and infections. This is plainly a reflection of the aging immune system, referred to as immune senescence, related to increased mortality and morbidity in the aged population. The immune cells mostly affected by aging are naïve T cells [9]. Yet the number of memory cells is proportionally increased. The process of T cell-mediated immunity becoming deteriorated gradually occurs, and both extrinsic and intrinsic

Rather than being influenced by bone marrow aging, age-related deterioration of T cell-mediated immunity is influenced by the thymic involution. Both are, however, seated to serve as co-directors of this process. When the thymus undergoes aging, its architecture does not remain well defined. Cellular changes associated with thymic involution include reduction in the number of thymic epithelial cells and thymocytes in contrast to an increase in perivascular spaces and adipose tissue. Aging will affect the bone marrow in parallel to the thymus, making the quantity and quality of progenitor T cells that migrate from the bone marrow to the thymus go down. When "progenitor T cells" are not inputted to the "thymus" machine, then the output "naïve T cells" would not be logic anymore. In this manner, aging causes a decline in naïve T cells exported from the thymus to the periphery, and conse-

Thymic involution is characterized by a continuous flow from the first year of life that gets pronounced at puberty and during pregnancy. After puberty, the thymus gradually decreases in size, weight, and cellularity as we age, and by the seventh decade of life, the thymic epithelial space drops to less than 10 percent of total tissue. This fact that the thymus feels old when the levels of sex steroids and hormones rise [9] provides, as a result, a role for sex steroids in the aging of the thymus. It also will open our eyes to see sex steroid ablation as a potential means of regenerating the thymus and consequently reversing immune senescence. There is reasonable evidence to believe that the prevention and/or reversal of thymic

tolerant to pathogens, and self-reactive T cells [8].

effector T cells that recirculate between peripheral tissues [8].

quently memory T cells will predominate in the periphery.

*3.2.2 The thymus has the ability to sustain life*

**3.2 The role of thymic involution in the aging immune system**

*3.1.2 The thymus can cope with infection*

*3.2.1 The thymus gets old*

factors may play a role [10].

**4**

Amene Saghazadeh1,2 and Nima Rezaei1,3,4\*

1 Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences (TUMS), Tehran, Iran

2 Systematic Review and Meta-analysis Expert Group (SRMEG), Universal Scientific Education and Research Network (USERN), Tehran, Iran

3 Department of Immunology, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran

4 Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran

\*Address all correspondence to: rezaei\_nima@yahoo.com

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
