As part of the aging process, the thymus undergoes progressive involution or atrophy in most vertebrates, exhibiting not only morphological changes, but also a functional decline resulting in, significantly lowered thymic output.
The thymus begins to shrink after puberty and its capacity to produce immune cellsgradually reduces, but may not completely diminish. Also, while the majority of T-cells mature in the thymus, there have been reports of T-cell maturation in the liver and intestines.
The thymus begins to shrink after puberty and its capacity to produce immune cellsgradually reduces, but may not completely diminish. Also, while the majority of T-cells mature in the thymus, there have been reports of T-cell maturation in the liver and intestines.
T-cells are named for the thymus where T-lymphocytes migrate from the bone marrow to mature. Its regression has been linked to the reduction in immunosurveillance and the rise of infectious disease and cancer incidence in the elderly (in some cases risk is inversely proportional to thymus size).
(By restoring thymic function, we would repair the defects in negative selection and rebalance tTreg generation. Currently, there are several strategies for rejuvenation of thymic involution in the literature, some of which target systemic T cell immunity and others focus on the thymus itself).
The reference is https://www.google.com/url?sa=t&source=web&rct=j&url=https://immunityageing.biomedcentral.com/articles/10.1186/s12979-020-0173-8&ved=2ahUKEwil2tOp9orpAhVGyqQKHZXpCCMQFjAQegQIBBAB&usg=AOvVaw2TBKX1sCeHopu4feYw_yMF&cshid=1588070513295
T lymphocyte (T cell) development and selection occurs in the thymus [29]. Included in this process is central tolerance establishment (Fig. 1, #1 and #2 top left), which occurs via two mechanisms. First is thymocyte negative selection, during which the majority of self (auto)-reactive T cells are depleted from the repertoire via apoptosis [30]. Second is the generation of CD4 single positive (CD4SP) FoxP3+ regulatory T (Treg) cells [31], whose primary function is to suppress T cell-mediated self-reactivity and preserve immune homeostasis in the periphery [32]. These arms of central T cell tolerance work in tandem, and Treg cells most likely compensate for imperfections of negative selection, as some self-reactive T cells escape negative selection [33]. With age, however, the atrophied thymus declines in its capacity to establish central tolerance, thereby, causing increased self-reactive T cells to escape to the periphery and participate in the process of inflammaging.
You may find discussions of rebound thymic hyperplasia of interest. Thymic hyperplasia occurs in patients with myasthenia gravis and other autoimmune disorders. Thymic size also varies with age, corticosteroid use, infections, and inflammatory disease. Rebound thymic hyperplasia has also been described following chemotherapy and most notably stem cell transplantation. Thymic hyperplasia is suggested to occur following lymphocyte depletion by chemotherapy, radiotherapy or intense corticosteroid therapy.