The Opsonization is a process of the immune system. Antibodies or proteins of the complement system bind to cells foreign to the body and mark them so that the phagocytes can find them. A lack of opsonization equates to a weak immune system and often corresponds to a hereditary lack of certain complement factors.
What is opsonization?
The medical term of Opsonization or opsonization comes from the Greek and literally means something like "food". In the human body, opsonization is an immunological mechanism.
The immune system protects people from foreign cells and pathogens. Foreign cells are recognized as such by the immune system and marked by antibodies or the so-called complement system. This marking enables the defense reaction.
The marking processes correspond to the opsonization. They take place on the surface of foreign cells such as viruses and bacteria. After opsonization, immunological cells such as granulocytes and macrophages recognize the invading microorganisms as foreign and go over to phagocytosis (defense).
An opsonin antibody is immunoglobulin G, which, with its Fc component, binds to the Fc receptors of phagocytes and thus stimulates phagocytosis. In the complement system, C3b is the most important opsonin. It binds to the CR1 receptors on monocytes, phagocytes, neutrophils, macrophages and some dendritic cells. In this way, it initiates phagocytosis of a particle without the need for specific antibodies.
This means that opsonization is an important process of the innate immune system and can sometimes take place independently of learned immune responses. Opsonization often takes place at the same time through antibodies and the complement system.
Function & task
With opsonization, pathogens such as bacteria are identified for the phagocytes of the immune system. The immunological phagocytes or macrophages eat pathogens faster and more effectively.
One possibility of opsonization is the binding of antibodies. The opsonin antibodies belong almost exclusively to the IgG class. In most cases it is IgG1 and IgG2. These antibodies consist of two heavy and two light protein chains and are Y-shaped. At their short ends they have binding sites that bind to the surface structures of foreign cells and haptens. The antigen-binding part is called the Fab fragment. The immunoglobulins mark the foreign cells for the immune system and make them easier to find and attack.
The IgG antibodies are part of the secondary immune response and are specific immune cells that are only produced through initial contact with antigens and the sensitization of the immune system achieved in this way. In the primary immune response, the antigen labeling usually takes place through the complement system. This is a plasma protein system that is activated on the surfaces of microorganisms.
The complement system contains over 30 proteins that have cell-destroying properties themselves. With opsonization, the proteins of the complement system cover the surface of the pathogen and enable the phagocytes to recognize and destroy them. Several glycoproteins are involved in the classic way of complement system activation.
This is to be distinguished from the lectin pathway, in which the mannose-binding lectin binds to N-acetylglucosamine on pathogenic surfaces and thus activates the MBL-associated serine protease. The alternative way of the complement system activation is triggered by the spontaneous decay of an unstable complement factor. The first way is usually mediated via antibodies. The second way is based on lectin mediation. The third and alternative way corresponds to a spontaneous reaction that is completely independent of antibodies.
All three pathways stimulate the complement system to allow C3 convertases to bind to the surface of foreign cells. This process leads to a so-called cleavage cascade, which triggers a chemotactic attraction of macrophages. Phagocytosis, which leads to the lysis of foreign cells, takes place.
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A lack of complement factors in particular has serious effects on the immunological constitution. If the doctor determines that the values of the complement system are low, this may be due to an immune complex disease, for example.
Diseases such as acute pancreatitis may be related to the phenomenon. This is an acute inflammation of the pancreas. Autoimmune hemolytic anemias can also be responsible for lowered complement system values. In these diseases, antibodies are directed against the body's own erythrocytes and thus trigger anemia.
Just as often, a deficiency in complement factors is caused by dermatosis. Diseases such as a blistering skin condition or autoimmune blistering dermatosis are possible causes. A lack of complement factors is also a symptom of glomerulonephritis such as post-streptococcal GN or SLE nephritis, which are favored by complement consumption.
Collagenoses and thus inflammatory rheumatic diseases in the connective tissue are also often associated with deficiency symptoms of the complement system. The same applies to cryoglobulinaemia and thus chronically recurring immune diseases of the vessels. These diseases can be diagnosed by detecting abnormal and cold-precipitating serum proteins. On the other hand, a lack of complement factors can also indicate damage to the liver parenchyma, inflammation of blood vessels, or rheumatoid arthritis.
Diseases not caused by immune complexes, with associated deficiency symptoms in the complement system, are all chronic inflammations and tumors. Sometimes the deficiency symptoms are also genetic. For example, a C4 deficiency can have a hereditary and thus hereditary basis. The most common hereditary defect of the complement system is a deficiency in C1 inhibitors, which causes angioedema.
Patients with complement system defects particularly often suffer from the main symptom of bacterial infection. Your complement system is limited in opsonization activity. In this way, invading pathogens are found and destroyed less effectively and less quickly by the immunological phagocytes. This phenomenon is equivalent to a weak immune system, but can be symptomatically associated with autoimmune-like diseases.
