Abstract
The thymus is a vital organ of the immune system that plays an essential role in thymocyte development and maturation. Thymic atrophy occurs with age (physiological thymic atrophy) or as a result of viral, bacterial, parasitic or fungal infection (pathological thymic atrophy). Thymic atrophy directly results in loss of thymocytes and/or destruction of the thymic architecture, and indirectly leads to a decrease in naïve T cells and limited T cell receptor diversity. Thus, it is important to recognize the causes and mechanisms that induce thymic atrophy. In this review, we highlight current progress in infection-associated pathogenic thymic atrophy and discuss its possible mechanisms. In addition, we discuss whether extracellular vesicles/exosomes could be potential carriers of pathogenic substances to the thymus, and potential drugs for the treatment of thymic atrophy. Having acknowledged that most current research is limited to serological aspects, we look forward to the possibility of extending future work regarding the impact of neural modulation on thymic atrophy.
Highlights
Senility postponement is a topic of perennial importance for scientists
Thymic atrophy induced by pathogens is a common phenomenon in infectious diseases
Thymic atrophy caused by different pathogens presents certain similarities, and has differences
Summary
Senility postponement is a topic of perennial importance for scientists. Aging inevitably leads to tissue damage and organ dysfunction, and individuals become more sensitive to infections, tumors and other diseases as they age. The medulla is made of thymic epithelial cells, single positive (SP) thymocytes and macrophages. Age-associated thymic atrophy leads to decreased naive T lymphocytes, which is followed by a series of immune sequelae mentioned above [10]. This series of age-related changes that affect the immune system are defined as immunosenescence [15], whose main features are defective immune responses, increased systemic inflammation [16] and increased susceptibility to cancer [17]. HPPRRSV attenuated strain shows a reduced ability to induce thymocyte atrophy [113], indicating that pathogenicity is positively correlated with the degree of thymic atrophy. A) Degree of thymocyte apoptosis is positive correlated with M-MuLV leukemogenesis
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