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 turns 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 cell that ingest invading viruses and bacteria.
The thymus gland is at its largest 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.
During the eighth week of gestation, the thymus descends and takes its final position in the antero superior 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, and this is how the thymocytes come into contact with the thymus gland, and the lymphoid tissue unites with the framework of epithelial cells of the scam.
The growth and development of the thymus continues until puberty. There are two different types of cells within the thymus, namely 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 they are 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 in 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.
Parallel to the gland on its left and right side are the phrenic nerves.
The two distinct lobes of the thymus are connected in the midline by an isthmus.
There are numerous thymic arteries that follow the course of the interlobular septa and can enter the tissues of the organ.
In the thymic cortex, the arteries form a series of complex arches and in association with reticular endothelial cells and white blood cells (lymphocytes and macrophages) form the thymus barrier in the blood.
Thymic capillaries have non-fenestrated endothelium and a thick basal lamina that make it impervious to proteins.
Blood drains into the medullary veins. The blood supply to the thymus comes from the interior thoracic arteries as well as the superior and inferior arteries of the thyroid.
Drainage is to the left innominate vein, as well as the superior, middle, and inferior thyroid veins.
The thymus has no afferent lymphatics. The lymph nodes located near the mammary gland drain to the thymus, that is, 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 is made up of inner and outer layers of collagen and reticular fibers, lymphocytes are in between.
This is the outer portion of the thymus gland and contains a large number of 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 and dendritic cells, type IV epithelial reticular cells are also present here.
This is the central portion, and it is 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.
Some development of thymocytes, in the last stage, 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 negative selection.
The medulla is therefore the site where the vast majority of negative selection takes place.
The thymus is the place where hematopoietic precursor cells mature into T cells.
The pro-thymocytes will 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 that are 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 own cell surfaces, which are essential for the adaptive immune system to recognize pathogens and therefore able to recognize the person’s own 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 negative 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, there is a large number of T cells accumulated during the first years of life, so that in adulthood the organ is largely obsolete and degrades.
The gland continues to have 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. 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, 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 a worsening of tiredness as the day progresses and weakness in the muscles.
Symptoms are the result of 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 therefore reduce the number of autoantibodies, is also a treatment option.
The prognosis for the condition is generally good. If the drug is well absorbed, the quality of life is good too.
Patients require monitoring for the first few years as many patients have a myasthenia crisis within this time.
Di George syndrome (22q deletion)
In this syndrome there is an aplasia of the thymus that causes a profound detrimental effect on the development of T cells, causing immunodeficiency and, therefore, increased susceptibility to infections.
There are no other white blood cells affected. The other features of this syndrome are cardiac abnormality, cleft palate, and hypoparathyroidism .