Opsonization is a process of the immune system. In this process, antibodies or proteins of the complement system bind to cells foreign to the body and label them to make them detectable by phagocytes. Lack of opsonization is tantamount to a defense deficiency and often corresponds to a hereditary deficiency of certain complement factors.
What is opsonization?
Opsonization is a process of the immune system. In this process, antibodies or proteins of the complement system bind to cells foreign to the body and label them to make them detectable by phagocytes. The medical term opsonization or opsonization comes from the Greek and literally means “feeding”. In the human body, opsonization is an immunological mechanism. The immune system protects humans 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 labeling enables the defense reaction. The labeling processes correspond to 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 invaded microorganisms as foreign to the body and proceed to phagocytosis (the defense). An opsonin antibody is immunoglobulin G, which binds to the Fc receptors of phagocytes with its Fc moiety and thus stimulates phagocytosis. In the complement system, C3b is the most important opsonin. It binds to the CR1 receptors on monocytes, phagocytes, neutrophil granulocytes, macrophages and some dendritic cells. Thus, it initiates phagocytosis of a particle without the need for specific antibodies. Thus, opsonization is an important process of the innate immune system and may occur in part independently of learned immune responses. Often, opsonization also occurs simultaneously by antibodies and the complement system.
Function and task
Opsonization involves labeling pathogens, such as bacteria, for the phagocytes of the immune system. As a result, the immunological phagocytes or macrophages eat pathogens more quickly and effectively. One way opsonization works is by binding antibodies. Opsonin antibodies belong almost exclusively to the IgG class. In most cases, they are IgG1 and IgG2. These antibodies consist of two heavy and two light protein chains and are Y-shaped. At their short ends they carry binding sites that bind to the surface structures of foreign cells and haptens. The antigen-binding part is called Fab fragment. The immunoglobulins thus mark the foreign cells for the defense system, making them easier to find and attack. The IgG antibodies belong to the secondary immune response and are specific immune cells that are produced only by an initial contact with antigens and the sensitization of the immune system thus achieved. In the primary immune response, antigen labeling usually takes place through the complement system. This is a plasma protein system that comes to activation on the surfaces of microorganisms. The complement system contains over 30 proteins that themselves have cell-destroying properties. During opsonization, the proteins of the complement system cover the surface of the pathogens, allowing phagocytes to recognize and destroy them. Several glycoproteins are involved in the classical pathway of complement system activation. This must be distinguished from the lectin pathway, in which the mannose-binding lectin binds to N-acetylglucosamine on pathogenic surfaces, thereby activating the MBL-associated serine protease. The alternative pathway of complement system activation is triggered by spontaneous decay of an unstable complement factor. Thus, the first pathway is usually mediated by antibodies. The second pathway is based on lectin mediation. The third and alternative pathway corresponds to a spontaneous response 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 initiates a chemotactic attraction of macrophages. Thus, increased phagocytosis takes place, leading to lysis of the foreign cells.
Diseases and disorders
Specifically, a deficiency of complement factors has serious effects on the immunologic constitution.If the physician detects lowered values with regard to the complement system, this may be due to an immune complex disease, for example. Diseases such as acute pancreatitis may be associated with the phenomenon. This is an acute inflammation of the pancreas. Autoimmune hemolytic anemias may also be responsible for lowered complement system levels. In these diseases, antibodies are directed against the body’s own erythrocytes and thus trigger anemia. Just as often, a deficiency in complement factors underlies a dermatosis. Diseases such as a blistering skin disease or a blistering autoimmune dermatosis are possible causes. Deficient complement factors are also a symptom of glomerulonephritis such as poststreptococcal GN or SLE nephritis, which are favored by complement depletion. Collagenoses and thus inflammatory rheumatic diseases in the connective tissue are also frequently associated with deficiency symptoms of the complement system. The same applies to cryoglobulinemias and thus chronically recurring immune diseases of the vessels. These diseases can be diagnosed by the detection of abnormal and cold-precipitating serum proteins. On the other hand, deficiency of complement factors may also indicate liver parenchymal damage, inflammation of blood vessels, or rheumatoid arthritis. Non-immune complex-related diseases, with associated deficiencies in the complement system, include all chronic inflammations and tumors. Sometimes the deficiency symptoms are genetic. For example, C4 deficiency can have a hereditary and therefore inherited basis. The most common hereditary complement system defect is a deficiency of C1 inhibitors, which causes angioedema. Patients with complement system defects particularly often suffer from the leading symptom of bacterial infection. Their complement system is impaired in opsonizing activity. Thus, invading pathogens are found and destroyed less effectively and less quickly by the immunological phagocytes. This phenomenon is tantamount to a defense deficiency, but symptomatically it may be equally well associated with autoimmune-like diseases.
