Thymusatrophie

Thymus atrophy, also known as thymic involution, is the progressive reduction of thymic tissue. The thymus is a primary lymphoid organ where T cells mature. With advancing age, the thymus decreases in size and is increasingly replaced by fat, leading to a decline in thymic output of naïve T cells and a narrowing of the T cell receptor repertoire. This process begins after puberty and continues into adulthood, contributing to immunosenescence.

Causes and contributing factors include the normal, age-related involution, as well as conditions and treatments that accelerate tissue loss. Malnutrition, chronic illness, severe physiological stress, and medical therapies such as chemotherapy, radiation, and high-dose corticosteroids can hasten thymic shrinkage. Congenital thymic hypoplasia (for example, in DiGeorge syndrome) reflects reduced thymic tissue from birth, which is not a consequence of age-related atrophy.

Diagnosis and pathology are typically inferred from clinical context and, when available, imaging or laboratory measures. Imaging can show a smaller thymus that is less phy­sically prominent on chest CT or MRI in adults. Histologically, thymic involution is characterized by a diminished thymic cortex with increased adipose tissue, accompanied by reduced thymopoiesis and T cell production. Peripheral markers, such as reduced T cell receptor excision circles, can indicate diminished thymic output.

Clinical implications include an age-associated rise in susceptibility to infections and weaker responses to vaccination due to diminished production of naïve T cells. There is no standard treatment to reverse physiological thymic atrophy; management focuses on overall immune health, infection prevention, adequate nutrition, and appropriate vaccination, while underlying conditions are treated as needed.