Its functions were not well understood until recent decades when its central role in the body’s immune system was recognized.
The thymus is a small gland located in the chest cavity just behind the upper end of the breastbone.
The thymus gland processes many of the white blood cells that are made in the bone marrow and turn these cells into T lymphocytes.
These cells play a crucial role in the body’s defense against infection.
They stimulate the production of antibodies by other lymphocytes and also stimulate the growth and activity of phagocytes, which are a form of scavenger cells that ingest invading viruses and bacteria.
The thymus gland is at its most significant in the infant and regresses in size over the years.
This reduction in size leads to reduced function in the gland.
Origin and development of the thymus gland
The thymus gland has a double embryonic origin.
The thymic epithelium develops during the sixth week of gestation from the ventral diverticular epithelium of the third pharyngeal bag together with the thyroid and parathyroid gland.
It extends posterolaterally into the surrounding mesoderm as two flask-like structures.
The cells that line these flask-like structures lead to further proliferation and are eventually surrounded and invaded by the mesoderm.
It shares it with the thyroid and parathyroid glands.
The thymus descends during the eighth week of gestation and takes its final position in the anterosuperior mediastinum.
It merges with its counterpart from the opposite side.
At the end of development, the precursor cells of the hematopoietic bone marrow (mesenchymal origin) migrate towards the thymus. This is how the thymocytes come into contact with the thymus gland. The lymphoid tissue unites with the framework of epithelial cells of the scam.
The growth and development of the thymus continue until puberty. There are two different types of cells within the thymus: the lymphoid cells (thymocytes) and the reticular epithelial cells.
In children, T cells densely occupy the cortex of the thymus.
As T cells develop, they pass into the marrow before being released into the circulation.
At the age of adolescence, the thymus gland begins to atrophy.
Many factors play their role in the involution process, the level of circulating hormones in the blood, that is, sex hormones also cause the gland to atrophy, and it is replaced by fat.
The thymus gland is a soft, bilobed organ that is encapsulated.
It is found in the upper mediastinum and the anterior part of the lower mediastinum, near the pericardium, anterior to the great vessels of the heart, and deep to the sternum.
It extends from the level of the thyroid gland of the lower poles to the fourth costal cartilage.
The phrenic nerves are parallel to the gland on its left and right side.
The two distinct lobes of the thymus are connected in the midline by an isthmus.
Numerous thymic arteries follow the course of the interlobular septa and can enter the organ’s tissues.
In the thymic cortex, the arteries form a series of complex arches. They are associated with reticular endothelial cells and white blood cells (lymphocytes and macrophages) from the thymus barrier in the blood.
Thymic capillaries have non-fenestrated endothelium and a thick basal lamina that make them impervious to proteins.
Blood drains into the medullary veins. The blood supply to the thymus comes from the anterior thoracic arteries and the superior and inferior arteries of the thyroid.
Drainage is to the left innominate vein and the superior, middle, and inferior thyroid veins.
The thymus has no afferent lymphatics. The lymph nodes near the mammary gland drain to the thymus, the parasternal, brachiocephalic and tracheobronchial.
Nerve supply to the thymus is minimal and originates from the vagus nerves and the sympathetic nervous system, extending into the thymus via postganglionic noradrenergic fibers.
The thymus is covered by a capsule of connective tissue, the septa of which penetrate the tissue and divide it into incomplete lobes.
Each lobe has a peripheral dark area called the cortex and a lighter middle area called the medulla.
The capsule comprises inner and outer layers of collagen and reticular fibers; lymphocytes are in between.
This is the outer portion of the thymus gland and contains many small, densely packed precursors of T lymphocytes (thymocytes).
It also contains epithelial reticular cells and macrophages. The blood vessels of the thymus are also found within this network of epithelial reticular cells.
The cortex is where the early stages of thymocyte development occur and where the rearrangement of receptor genes takes place on the surface of T cells.
It had numerous blood vessels, little connective tissue, and mature T lymphocytes.
B cells, dendritic cells, and type IV epithelial reticular cells are also present here.
This is the central portion, where the network of reticular endothelial cells is most dense and where the lymphoid cells are less.
There are also a series of concentric bodies known as Hassall’s corpuscles.
They are flattened epithelial reticular cells arranged concentrically and filled with keratin filaments.
Also, within these corpuscles is a central mass of a few granule cells.
In the last stage, some development of thymocytes also occurs in the medulla.
The thymocytes located here have passed through the cerebral cortex and have undergone receptor gene rearrangement and positive selection, with a small amount of adverse selection.
The medulla is, therefore, the site where the vast majority of adverse selection takes place.
The thymus is the place where hematopoietic precursor cells mature into T cells.
The pro-thymocytes migrate from the bone marrow and enter the thymus gland at the corticomedullary junction.
Once the maturation process is complete, these T cells enter the circulation and form the basis of the adaptive immune system.
T cells have receptors generated from a random selection of the gene segment.
Initially, a process known as positive selection works (which occurs in the cortex), which checks whether the developing T cell can recognize the proteins of the major histocompatibility complex.
This is a set of proteins on a person’s cell surfaces, which are essential for the adaptive immune system to recognize pathogens and therefore recognize the person’s cells from foreign cells.
Cells that do not perform this reaction or perform it too weakly are prevented from entering further development.
The next stage is adverse selection, where T cells undergo the process of interaction with thymic dendritic cells.
Those cells with a high level of self-reactivity are killed to reduce the likelihood of autoimmune reactions.
As a result of this process, many T cells accumulate during the first years of life so that in adulthood, the organ is obsolete mainly and degrades.
The gland continues to have an endocrine function.
T cells divide into helper T cells and cytotoxic T cells.
Cytotoxic T cells have CD8 proteins on their surface, and they bind to infected cells and destroy them directly.
Helper T cells receive information about the pathogen from antigen-presenting cells (B cells and macrophages) and coordinate the immune response, releasing cytokines that cause further division of white blood cells, leading to the production of memory B cells for infections—the future of that pathogen.
This is a rare tumor that arises from the epithelial cells of the thymus gland.
It has an association with myasthenia gravis in 20% of patients.
Other risk factors include old age and Asian ethnicity.
The symptoms are caused by the expansion of the tumor that compresses the surrounding structures, for example, compression of the vena cava, dysphagia, cough, and chest pain, among others.
Diagnosis is made by CT scan, and treatment is surgery with additional chemotherapy and radiation therapy in some cases.
This is an autoimmune condition characterized by worsening tiredness as the day progresses and weakness in the muscles.
Symptoms result from autoimmune destruction of acetylcholine receptors found at postsynaptic neuromuscular junctions due to autoantibodies.
Diagnosis is made with the edrophonium test or a placebo (inactive).
Treatment is with long-acting acetylcholinesterase inhibitors as well as immunosuppressive drugs.
Surgery to remove the thymus gland and reduce the number of autoantibodies is also a treatment option.
The prognosis for the condition is generally reasonable. If the drug is well absorbed, the quality of life is good.
Patients require monitoring for the first few years as many patients have a myasthenia crisis.
Di George syndrome (22q deletion)
In this syndrome, aplasia of the thymus causes a profound detrimental effect on the development of T cells, causing immunodeficiency and, therefore, increased susceptibility to infections.